Updated on 2026/04/16

写真a

 
YAMAMOTO Koji
 
Organization
School of Medicine Medical Course Basic Medicine Physiology[Autonomous Function]
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Degree

  • 博士 (医学) ( 2011.3   神戸大学 )

  • 博士（医学） ( 神戸大学 )

Research Areas

  • Life Science / Gastroenterology

Education

  • Kobe University   Graduate School, Division of Medical Sciences

    - 2011.3

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    Country： Japan

  • 神戸大学 大学院医学系研究科博士課程修了

    - 2011.3

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Papers

  • Splicing Factor 3a Subunit 1 Promotes Colorectal Cancer Growth via Anti-Apoptotic Effects of Syntaxin12

    Takahiro Sasaki, Hiroaki Konishi, Tatsuya Dokoshi, Aki Sakatani, Hiroki Tanaka, Koji Yamamoto, Keitaro Takahashi, Katsuyoshi Ando, Nobuhiro Ueno, Shin Kashima, Kentaro Moriichi, Hiroki Tanabe, Toshikatsu Okumura, Mikihiro Fujiya

    International Journal of Molecular Sciences   27 ( 3 )   1195 - 1195   2026.1

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    Publishing type：Research paper (scientific journal)   Publisher：MDPI AG  

    RNA dysregulation mediated by aberrant RNA-binding proteins (RBPs) is closely associated with tumorigenesis. However, the tumorigenic mechanisms of each RBP remained unclear. In this study, we demonstrate that downregulation of Splicing factor 3A1 (SF3A1) markedly suppressed the proliferation of colorectal cancer (CRC) cells, with minimal cytotoxicity observed in non-cancerous epithelial cells. The tumor-promoting function of SF3A1 was further validated in an HCT116 xenograft mouse model. Multiple apoptosis assays—including TdT-mediated dUTP nick end labeling (TUNEL) staining, poly-ADP-ribose polymerase (PARP) immunoblotting, and caspase-3/7 activity measurements—showed that SF3A1 inhibited apoptotic signaling in CRC cells. Transcriptome analysis, combined with RNA-immunoprecipitation (RIP), identified Syntaxin 12 (STX12) as a downstream effector of SF3A1. Knockdown of STX12 induced apoptosis in CRC cells but had no effect on the viability of non-cancerous HCEC-1CT epithelial cells. Furthermore, STX12 mRNA levels were significantly reduced following SF3A1 knockdown, indicating that SF3A1-mediated stabilization of STX12 contributes to apoptosis resistance in CRC cells. Collectively, our findings establish that SF3A1 promotes CRC progression by stabilizing STX12 mRNA and selectively inhibiting apoptosis in malignant cells, thereby identifying the SF3A1–STX12 regulatory axis as a novel and selective therapeutic target for CRC.

    DOI： 10.3390/ijms27031195

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  • Peptidoglycan from <i>Bifidobacterium bifidum</i> G9-1 induces IgA secretion in Peyer’s patch-derived cells

    Hiroaki KONISHI, Koji YAMAMOTO, Aki SAKATANI, Tatsuya DOKOSHI, Yutaka MAKIZAKI, Yoshiki TANAKA, Hiroshi OHNO, Kentaro MORIICHI, Mikihiro FUJIYA

    Bioscience of Microbiota, Food and Health   45 ( 1 )   79 - 83   2026

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    Publishing type：Research paper (scientific journal)   Publisher：BMFH Press  

    DOI： 10.12938/bmfh.2025-040

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  • hsa_circ_0015388 Reduces Macrophage Derived Reactive Oxygen Species in Crohn's Disease. International journal

    Yuya Sugiyama, Hiroaki Konishi, Tatsuya Dokoshi, Hiroki Tanaka, Yu Kobayashi, Takahiro Sasaki, Koji Yamamoto, Aki Sakatani, Keitaro Takahashi, Katsuyoshi Ando, Nobuhiro Ueno, Shin Kashima, Kentaro Moriichi, Hiroki Tanabe, Toshikatsu Okumura, Mikihiro Fujiya

    Inflammatory bowel diseases   2025.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND: Crohn's disease (CD) is a refractory inflammatory bowel disease with an unclear etiology. CircularRNA (circRNA) has been highlighted as a novel class of functional noncoding RNAs associated with the pathogenesis of various diseases. However, the functions of circRNA in CD remain unclear. METHODS: Biopsies were obtained from noninflammatory sites in the terminal ileum of the CD group (n = 4) and non-CD group (n = 4) and analyzed for circRNA expression using RNA sequencing. The significantly altered circRNAs were validated in the CD group (n = 45) and non-CD group (n = 15) using quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Transcriptome analysis was conducted using circRNA-downregulated macrophage-like THP-1 cells. Reactive oxygen species (ROS) levels, cytokine mRNA expression, phagocytosis, and migration were evaluated in circRNA-downregulated THP-1 cells. RESULTS: CircularRNA sequencing analysis revealed significant differences in 31 circRNAs between the CD group and non-CD group. Quantitative reverse transcriptase-polymerase chain reaction analysis for each circRNA demonstrated significant upregulation of hsa_circ_0015388 in the CD group. Hsa_circ_0015388 was expressed in THP-1 cells, but not in HCEC-1CT and Caco-2/bbe. Transcriptome analysis in THP-1 cells transfected with scramble or hsa_circ_0015388 siRNA (small interfering RNA) showed a significant alteration in innate immune response related pathway. Reactive oxygen species production was significantly increased in the hsa_circ_0015388 downregulated THP-1 cells. Reactive oxygen species induction in the hsa_circ_0015388 knocked down THP-1 was diminished by the inhibition of TNFSF10. CONCLUSION: A comprehensive analysis of circRNA expression revealed that 31 circRNAs were dysregulated in the CD group. Hsa_circ_0015388 is expressed in macrophages and negatively regulates ROS function inhibiting the TNFSF10 pathway. This study first revealed that hsa_circ_0015388 plays a role in the pathogenesis of CD by suppressing ROS production in macrophages.

    DOI： 10.1093/ibd/izae317

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  • Probiotic-derived ferrichrome induces DDIT3-mediated antitumor effects in esophageal cancer cells. International journal

    Takehito Kunogi, Hiroaki Konishi, Aki Sakatani, Kentaro Moriichi, Chikage Yamamura, Koji Yamamoto, Shin Kashima, Katsuyoshi Ando, Nobuhiro Ueno, Hiroki Tanaka, Toshikatsu Okumura, Mikihiro Fujiya

    Heliyon   10 ( 6 )   e28070   2024.3

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    Language：English   Publishing type：Research paper (scientific journal)  

    Esophageal cancer, which is common among the elderly, has the poorest prognosis among gastrointestinal cancers. Previously, we demonstrated that ferrichrome, produced by the probiotic Lactobacillus casei, exhibited anti-tumor effects in various gastrointestinal cancers, including colorectal and gastric cancers, with minimal effects on non-cancerous intestinal cells. However, it remains unclear whether ferrichrome exerts anti-tumor effects in esophageal cancer. A sulforhodamine B assay revealed that ferrichrome suppressed esophageal adenocarcinoma (OE33, OE19) and squamous cell carcinoma (KYSE70) cells. Ki-67 staining indicated that ferrichrome inhibited the proliferation of esophageal cancer cells. Cell cycle analysis showed that ferrichrome inhibited the DNA synthesis. TUNEL staining revealed that ferrichrome-induced DNA fragmentation. We also confirmed the cleavage of caspase-9 and PARP in ferrichrome-treated cells. Reverse transcription polymerase chain reaction demonstrated an increase in the mRNA of DNA damage-inducible transcript 3 (DDIT-3), a key regulator of programmed cell death, in ferrichrome-treated OE33 cells. In an in vivo OE33 xenograft model, intraperitoneal administration of 5-mg/kg ferrichrome for 14 days resulted in an almost complete inhibition of tumor growth. However, 14 days of intraperitoneal administration of 20-mg/kg 5-fluorouracil (5-FU), but not 20-mg/kg ferrichrome, induced weight loss and myelosuppression in both young and aged mice. Our findings indicate that ferrichrome induces DNA damage-inducible transcript-3, thereby producing anti-tumor effects, including cell cycle arrest and apoptosis, with minimal adverse effects in esophageal cancer cells. This illustrates the high potential of ferrichrome as an anti-tumor drug against esophageal carcinoma.

    DOI： 10.1016/j.heliyon.2024.e28070

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  • Incidence of post-transplant hepatitis B virus reactivation with the use of kidneys from donors with resolved hepatitis B virus infection. International journal

    Ren Yamada, Kenichi Morikawa, Kiyohiko Hotta, Daiki Iwami, Tatsu Tanabe, Sachiyo Murai, Nobuo Shinohara, Sonoe Yoshida, Shunichi Hosoda, Akinori Kubo, Yoshimasa Tokuchi, Takashi Kitagataya, Megumi Kimura, Koji Yamamoto, Masato Nakai, Takuya Sho, Goki Suda, Mitsuteru Natsuizaka, Koji Ogawa, Naoya Sakamoto

    Journal of viral hepatitis   29 ( 11 )   976 - 985   2022.11

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    Language：English   Publishing type：Research paper (scientific journal)  

    Donors with resolved hepatitis B virus (HBV) infection may be a solution for the organ shortage for kidney transplantation (KT). The purpose of this study was to clarify the current state of HBV markers after KT from donors with resolved HBV infection to HBV naïve recipients and the rate of HBV reactivation in recipients with resolved HBV infection. Furthermore, we investigated HBV covalently closed circular DNA (cccDNA) in transplanted organs from donors with resolved HBV infection and the capability of HBV replication in kidney cell lines. We retrospectively analysed the HBV status of 340 consecutive donors and recipients who underwent KT in a single centre. We prospectively measured cccDNA by real-time polymerase chain reaction in kidney biopsy specimens of 32 donors with resolved HBV infection. HBV reactivation was found in three recipients with resolved HBV infection (4.8%, 3/63) after KT. We analysed 45 cases of transplantation from donors with resolved HBV infection to HBV-naive recipients. One case (2.2%, 1/45) became seropositive for hepatitis B core antibody (anti-HBc) and in another case (2.2%, 1/45), HBV-DNA was detected qualitatively in an HBV naive recipient with a donor with resolved HBV infection. In the latter case, cccDNA was measured in the donor kidney during KT. HBV replication was observed in kidney cell lines with HBV plasmid transfection. In conclusion, the risk of reactivation in anti-HBc-positive donors is relatively low. However, post-transplant HBV monitoring should be conducted in all at-risk cases.

    DOI： 10.1111/jvh.13740

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  • Incidence of hepatitis B virus reactivation in kidney transplant patients with resolved hepatitis B virus infection. Reviewed

    Yamada R, Morikawa K, Hotta K, Iwami D, Tanabe T, Murai S, Shinohara N, Yoshida S, Hosoda S, Kubo A, Tokuchi Y, Kitagataya T, Kimura M, Yamamoto K, Nakai M, Sho T, Suda G, Natsuizaka M, Ogawa K, Sakamoto N.

    Journal of Virus Hepatitis   2022.8

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  • Oleoylethanolamide Ameliorates Dextran Sulfate Sodium-Induced Colitis in Rats. Reviewed

    Otagiri S, Ohnishi S, Ohara M, Fu Q, Yamamoto K, Yamamoto K, Katsurada T, Sakamoto N.

    Front Pharmacol.   2022.8

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  • Intravenous transplantation of amnion-derived mesenchymal stem cells promotes functional recovery and alleviates intestinal dysfunction after spinal cord injury. Reviewed

    Takamiya S, Kawabori M, Yamazaki M, Yamaguchi S, Tanimori A, Yamamoto K, Ohnishi S, Seki T, Konno K, Tha KK, Hashimoto D, Watanabe M, Houkin K, Fujimura M.

    PLoS One.   2022.7

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  • The potential of soluble CD14 in discriminating nonalcoholic steatohepatitis from nonalcoholic fatty liver disease. Reviewed

    Nakamura A, Yamamoto K (equally first author), Takeda R, Yamada R, Kubo A, Morikawa K, Ando S, Shimazaki T, Izumi T, Umemura M, Kitagataya T, Shigesawa T, Suzuki K, Kimura M, Nakai M, Sho T, Suda G, Natsuizaka M, Ogawa K, Ohnishi S, Sugiyama T, Takeda H, Sakamoto N.

    Hepatol Res.   2022.6

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  • Protocol for generating a mouse model of gastric MALT lymphoma and the identification of MALT lymphoma cell populations by immunostaining.

    Yamamoto K, Kondo Y, Sugiyama T, Sakamoto N.

    STAR Protocols   2022.3

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  • Protocol for generating a mouse model of gastric MALT lymphoma and the identification of MALT lymphoma cell populations by immunostaining. International journal

    Koji Yamamoto, Yasuyuki Kondo, Toshiro Sugiyama, Naoya Sakamoto

    STAR protocols   3 ( 1 )   101155 - 101155   2022.3

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    Helicobacter suis, a zoonotic infection-related bacterium, induces gastric mucosa-associated lymphoid tissue (MALT) lymphoma in humans and animals. However, a lack of suitable animal models complicates the detailed analysis of this disease. Here, we describe the generation of a gastric MALT lymphoma mouse model. We then detail the use of this model combined with an immunostaining protocol to identify the cell populations that constitute gastric MALT lymphoma. This protocol can be used to identify the constituent cells of human MALT lymphoma. For complete details on the use and execution of this profile, please refer to Yamamoto et al. (2021).

    DOI： 10.1016/j.xpro.2022.101155

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  • The potential of soluble CD14 in discriminating nonalcoholic steatohepatitis from nonalcoholic fatty liver disease. International journal

    Akihisa Nakamura, Koji Yamamoto, Rei Takeda, Ren Yamada, Akinori Kubo, Kenichi Morikawa, Sayaka Ando, Tomoe Shimazaki, Takaaki Izumi, Machiko Umemura, Takashi Kitagataya, Taku Shigesawa, Kazuharu Suzuki, Megumi Kimura, Masato Nakai, Takuya Sho, Goki Suda, Mitsuteru Natsuizaka, Koji Ogawa, Shunsuke Ohnishi, Toshiro Sugiyama, Hiroshi Takeda, Naoya Sakamoto

    Hepatology research : the official journal of the Japan Society of Hepatology   52 ( 6 )   508 - 521   2022.2

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    BACKGROUND AND AIMS: Although various noninvasive markers and prediction formulas for nonalcoholic steatohepatitis (NASH) have been reported, they are of value only in the diagnosis of the advanced fibrosis stage of NASH. In this study, we evaluated soluble CD14 (sCD14) as a diagnostic marker for discriminating NASH from nonalcoholic fatty liver disease (NAFLD) using an animal model and clinical specimens. METHODS: Serum sCD14 levels were measured in samples derived from mice with diet-induced NASH and patients using an enzyme-linked immunosorbent assay. Our cohort enrolled 126 patients with liver needle biopsy-proven NAFLD. RESULTS: The intestinal defense mechanism in NASH model mice was altered as a consequence of the unique gut environment. Elevated serum levels of sCD14 were observed in mice with diet-induced NASH, and the condition of the liver was exacerbated as a result of exposure to gut-derived endotoxin. We confirmed that the serum sCD14 levels in NAFL patients significantly differed from those in NASH patients. The area under the curve for distinguishing between NAFL and NASH was 0.891. Moreover, we found that serum sCD14 levels were weakly correlated with the inflammation grade based on the NAFLD activity score (NAS), the grade of fibrosis according to the Brunt fibrosis classification, and a positive correlation with the grade of ballooning based on NAS in patients with NAFLD. CONCLUSION: sCD14 could be a useful pathophysiological marker and diagnostic adjunct distinguishing NASH from NAFLD. The use of sCD14 may allow the screening and identification of high-risk groups for NASH development and support early therapeutic interventions.

    DOI： 10.1111/hepr.13757

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  • Intravenous transplantation of amnion-derived mesenchymal stem cells promotes functional recovery and alleviates intestinal dysfunction after spinal cord injury. International journal

    Soichiro Takamiya, Masahito Kawabori, Kazuyoshi Yamazaki, Sho Yamaguchi, Aki Tanimori, Koji Yamamoto, Shunsuke Ohnishi, Toshitaka Seki, Kotaro Konno, Khin Khin Tha, Daigo Hashimoto, Masahiko Watanabe, Kiyohiro Houkin, Miki Fujimura

    PloS one   17 ( 7 )   e0270606   2022

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    Spinal cord injury (SCI) is often accompanied by gastrointestinal dysfunction due to the disconnection of the spinal autonomic nervous system. Gastrointestinal dysfunction reportedly upregulates intestinal permeability, leading to bacterial translocation of the gut microbiome to the systemic circulation, which further activates systemic inflammation, exacerbating neuronal damage. Mesenchymal stem cells (MSC) reportedly ameliorate SCI. Here, we aimed to investigate their effect on the associated gastrointestinal dysfunction. Human amnion-derived MSC (AMSCs) were intravenously transplanted one day after a rat model of midthoracic SCI. Biodistribution of transplanted cells, behavioral assessment, and histological evaluations of the spinal cord and intestine were conducted to elucidate the therapeutic effect of AMSCs. Bacterial translocation of the gut microbiome was examined by in situ hybridization and bacterial culture of the liver. Systemic inflammations were examined by blood cytokines, infiltrating immune cells in the spinal cord, and the size of the peripheral immune tissue. AMSCs released various neurotrophic factors and were mainly distributed in the liver and lung after transplantation. AMSC-transplanted animals showed smaller spinal damage and better neurological recovery with preserved neuronal tract. AMSCs transplantation ameliorated intestinal dysfunction both morphologically and functionally, which prevented translocation of the gut microbiome to the systemic circulation. Systemic inflammations were decreased in animals receiving AMSCs in the chronic phase. Intravenous AMSC administration during the acute phase of SCI rescues both spinal damage and intestinal dysfunction. Reducing bacterial translocation may contribute to decreasing systemic inflammation.

    DOI： 10.1371/journal.pone.0270606

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  • The TLR4-TRIF-type 1 IFN-IFN-γ pathway is crucial for gastric MALT lymphoma formation after Helicobacter suis infection. Reviewed

    Yamamoto K, Kondo Y, Ohnishi S, Yoshida M, Sugiyama T, Sakamoto N.

    iScience   2021.9

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

  • The TLR4-TRIF-type 1 IFN-IFN-γ pathway is crucial for gastric MALT lymphoma formation after Helicobacter suis infection. International journal

    Koji Yamamoto, Yasuyuki Kondo, Shunsuke Ohnishi, Masaru Yoshida, Toshiro Sugiyama, Naoya Sakamoto

    iScience   24 ( 9 )   103064 - 103064   2021.9

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    Helicobacter suis, a zoonotic infection-related bacterium, can induce gastric mucosa-associated lymphoid tissue (MALT) lymphoma in humans and animals. Recently, we reported that the formation of gastric MALT lymphoma after H. suis infection is induced by interferon (IFN)-γ activation. Here, we revealed that activation of the Toll-like receptor (TLR) 4-Toll/IL-1 receptor domain-containing adapter-inducing interferon-β (TRIF) pathway after H. suis infection is associated with the production of type 1 IFNs (IFN-α, IFN-β) by gastric epithelial cells. Additionally, these type 1 IFNs interact with type 1 IFN receptors on gastric B cells, facilitating the secretion of IFN-γ and the activation of which is enhanced by positive feedback regulation in B cells. These results suggest that the TLR4-TRIF-type 1 IFN-IFN-γ pathway is crucial in the development of gastric MALT lymphoma after H. suis infection and may, therefore, represent a therapeutic target for the prevention of this condition.

    DOI： 10.1016/j.isci.2021.103064

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  • Lenvatinib suppresses cancer stem- Like cells in HCC by inhibiting FGFR1-3 signaling, but not FGFR4 signaling. Reviewed

    Shigesawa T, Maehara O, Suda G, Natsuizaka M, Kimura M, Shimazaki T, Yamamoto K, Yamada R, Kitagataya T, Nakamura A, Suzuki K, Ohara M, Kawagishi N, Umemura M, Nakai M, Sho T, Morikawa K, Ogawa K, Ohnishi S, Sugiyama M, Mizokami M, Takeda H, Sakamoto N.

    Carcinogenesis.   2021.2

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  • Tenofovir disoproxil fumarate modulates lipid metabolism via hepatic CD36/PPAR-alpha activation in hepatitis B virus infection. Reviewed

    Suzuki K, Suda G, Yamamoto Y, Furuya K, Baba M, Nakamura A, Miyoshi H, Kimura M, Maehara O, Yamada R, Kitagataya T, Yamamoto K, Shigesawa T, Nakamura A, Ohara M, Kawagishi N, Nakai M, Sho T, Natsuizaka M, Morikawa K, Ogawa K, Ohnishi S and Sakamoto N for the NORTE Study Group.

    J Gastroenterol.   2021.2

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  • Tenofovir-disoproxil-fumarate modulates lipid metabolism via hepatic CD36/PPAR-alpha activation in hepatitis B virus infection.

    Kazuharu Suzuki, Goki Suda, Yoshiya Yamamoto, Ken Furuya, Masaru Baba, Akinobu Nakamura, Hideaki Miyoshi, Megumi Kimura, Osamu Maehara, Ren Yamada, Takashi Kitagataya, Koji Yamamoto, Taku Shigesawa, Akihisa Nakamura, Masatsugu Ohara, Naoki Kawagishi, Masato Nakai, Takuya Sho, Mitsuteru Natsuizaka, Kenichi Morikawa, Koji Ogawa, Shunsuke Ohnishi, Naoya Sakamoto

    Journal of gastroenterology   56 ( 2 )   168 - 180   2021.2

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    BACKGROUND: Entecavir and tenofovir-disoproxil-fumarate are first-line nucleos(t)ide analogs (NA) for treatment of hepatitis B virus (HBV) infections; however, their long-term administration can impact extrahepatic organs. Herein, we sought to examine the effect of NA on lipid metabolism while also characterizing the associated mechanism. METHODS: A retrospective study was performed on HBV patients administered entecavir or tenofovir-disoproxil-fumarate. Patient clinical information, as well as their preserved serum samples obtained at baseline and 6-12 months after treatment initiation, were analyzed. A 1:1 propensity score matching was applied to the assignment of tenofovir-disoproxil-fumarate or entecavir treatment. Changes in serum cholesterol, including oxidized-LDL, were analyzed. Subsequently, in vitro analysis elucidated the mechanism associated with the effect of NAs on lipid metabolism. RESULTS: Administration of tenofovir-disoproxil-fumarate, not entecavir, to chronic HBV patients, decreased serum cholesterol levels, including non-HDL and oxidized-LDL, which are strongly associated with arteriosclerosis. In vitro analysis revealed that tenofovir-disoproxil-fumarate reduced supernatant cholesterol, and upregulated the scavenger receptor, CD36, in hepatocytes. Meanwhile, silencing of hepatic CD36 increased supernatant cholesterol and negated the cholesterol-reducing effect of tenofovir-disoproxil-fumarate in HepG2-cells. Reporter, microarray, and RT-PCR analyses further revealed that tenofovir-disoproxil-fumarate treatment activates PPAR-α-mediated signaling, and upregulates PPAR-α target genes, including CPT1 and CD36. Alternatively, silencing of PPAR-α reversed the effects of tenofovir-disoproxil-fumarate on CD36. CONCLUSIONS: Tenofovir-disoproxil-fumarate modulates lipid metabolism by upregulating hepatic CD36 via PPAR-α activation. Since dyslipidemia could be associated with arteriosclerosis and hepatocarcinogenesis, these discoveries provide novel insights into anti-HBV therapies, as well as the associated extrahepatic effects of NA.

    DOI： 10.1007/s00535-020-01750-3

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  • Prevalence, clinical course, and predictive factors of immune checkpoint inhibitor monotherapy-associated hepatitis in Japan. Reviewed

    Kitagataya T, Suda G, Nagashima K, Katsurada T, Yamamoto K, Kimura M, Maehara O, Yamada R, Shigesawa T, Suzuki K, Nakamura A, Ohara M, Umemura M, Kawagishi N, Nakai M, Sho T, Natsuizaka M, Morikawa K, Ogawa K, Ohnishi S, Komatsu Y, Hata H, Takeuchi S, Abe T, Sakakibara-Konishi J, Teshima T, Homma A, and Sakamoto N.　

    Journal of Gastroenterology and Hepatology.   2020.10

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  • Oleoylethanolamide Ameliorates Dextran Sulfate Sodium-Induced Colitis in Rats International journal

    Shinsuke Otagiri, Shunsuke Ohnishi, Masatsugu Ohara, Qingjie Fu, Koji Yamamoto, Keiko Yamamoto, Takehiko Katsurada, Naoya Sakamoto

    FRONTIERS IN PHARMACOLOGY   11   1277 - 1277   2020.8

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    DOI： 10.3389/fphar.2020.01277

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  • Lenvatinib suppresses cancer stem-like cells in HCC by inhibiting FGFR 1-3 signaling, but not FGFR4 signaling. Reviewed International journal

    Taku Shigesawa, Osamu Maehara, Goki Suda, Mitsuteru Natsuizaka, Megumi Kimura, Tomoe Shimazaki, Koji Yamamoto, Ren Yamada, Takashi Kitagataya, Akihisa Nakamura, Kazuharu Suzuki, Masatsugu Ohara, Naoki Kawagishi, Machiko Umemura, Masato Nakai, Takuya Sho, Kenichi Morikawa, Koji Ogawa, Shunsuke Ohnishi, Masaya Sugiyama, Masashi Mizokami, Hiroshi Takeda, Naoya Sakamoto

    Carcinogenesis   42 ( 1 )   58 - 69   2020.5

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    In hepatocellular carcinoma (HCC), a subset of cells defined by high CD44 and CD133 expression has been reported to possess cancer stem-like cell (CSC) characteristics and to be associated with a poor prognosis. Since the approval of the multi-kinase inhibitor, lenvatinib, for patients with unresectable HCC, two such inhibitors (sorafenib and lenvatinib) have been employed as first-line systemic chemotherapeutics for these patients. Based on differences in the kinase-affinity profiles between these two drugs, evidence has suggested that both exert different effects on HCC, although these differences are not fully characterized. In this study, using in vitro and a preclinical in vivo xenograft mouse model, we showed that lenvatinib alone (not sorafenib or the cytotoxic agent, 5-fluorouracil) diminished CD44High/CD133High CSCs in HCC. Furthermore, western blotting and RT-PCR analysis revealed that the expression of fibroblast growth factor receptor (FGFR)-1 to 4 differed between CD44High/CD133High CSCs and control cells. Analysis of the effects of selective FGFR inhibitors and FGFR small interfering RNAs on CSCs in HCC revealed that lenvatinib diminished CSCs in HCC by inhibiting FGFR1-3 signaling, however, FGFR4 signaling was not impacted. Finally, we showed that FGF2 and FGF19 were involved in maintaining CD44High/CD133High CSCs in HCC, potentially, via FGFR1-3. The findings provide novel mechanistic insights into the effects of lenvatinib on CSCs in HCC and provide clues for developing effective targeted therapies against CSCs in HCC.

    DOI： 10.1093/carcin/bgaa049

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  • Prevalence, clinical course, and predictive factors of immune checkpoint inhibitor monotherapy-associated hepatitis in Japan. Reviewed International journal

    Takashi Kitagataya, Goki Suda, Kazunori Nagashima, Takehiko Katsurada, Koji Yamamoto, Megumi Kimura, Osamu Maehara, Ren Yamada, Taku Shigesawa, Kazuharu Suzuki, Akihisa Nakamura, Masatsugu Ohara, Machiko Umemura, Naoki Kawagishi, Masato Nakai, Takuya Sho, Mitsuteru Natsuizaka, Kenichi Morikawa, Koji Ogawa, Shunsuke Ohnishi, Yoshito Komatsu, Hiroo Hata, Satoshi Takeuchi, Takashige Abe, Jun Sakakibara-Konishi, Takanori Teshima, Akihiro Homma, Naoya Sakamoto

    Journal of gastroenterology and hepatology   35 ( 10 )   1782 - 1788   2020.3

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    BACKGROUND AND AIM: Immune checkpoint inhibitors (ICI) have revolutionized anti-malignancy therapy and thus have been increasingly used. Although ICI may cause immune-related adverse events (irAE) in various organs, including the liver, the prevalence and predictive factors of irAE have not been clarified. METHODS: In this retrospective study, consecutive patients who had malignancies and were treated with ICI without other chemotherapeutic agents at Hokkaido University Hospital between 2014 and 2019 were screened. Patients were excluded if they were < 20 years old and had insufficient clinical data. RESULTS: Of the 233 patients screened, 202 patients met the inclusion criteria and were included in the analysis. The patients were aged 25-92 years, and 60.9% were male. The patients received nivolumab (n = 137), pembrolizumab (n = 45), ipilimumab (n = 17), atezolizumab (n = 2), and avelumab (n = 1). The prevalence of any grade and grade ≥ 3 irAE hepatitis was 8.4% (17/202) and 4.0% (8/202), respectively. irAE hepatitis occurred at a median duration of 42 days in any grade and 36 days in grade ≥ 3 after ICI initiation. The clinical course of grade ≥ 3 irAE hepatitis was generally favorable; however, 50% required corticosteroid treatment and two patients required additional mycophenolate mofetil. Female sex and history of ICI treatment were significantly associated with the incidence of grade ≥ 3 irAE hepatitis. CONCLUSIONS: Grade ≥ 3 irAE hepatitis was observed in 4.0% of the patients who were treated with ICI. Female sex and history of ICI treatment were significantly associated with the incidence of grade ≥ 3 irAE hepatitis.

    DOI： 10.1111/jgh.15041

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  • Entecavir treatment of hepatitis B virus-infected patients with severe renal impairment, including those on hemodialysis. Reviewed

    Suzuki K, Suda G, Yamamoto Y, Furuya K, Baba M, Kimura M, Maehara O, Shimazaki T, Yamamoto K, Shigesawa T, Nakamura A, Ohara M, Kawagishi N, Nakai M, Sho T, Natsuizaka M, Morikawa K, Ogawa K, Sakamoto N; NORTE Study Group.

    Hepatol Res.   2019.11

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  • Entecavir treatment of hepatitis B virus-infected patients with severe renal impairment and those on hemodialysis. Reviewed International journal

    Kazuharu Suzuki, Goki Suda, Yoshiya Yamamoto, Ken Furuya, Masaru Baba, Megumi Kimura, Osamu Maehara, Tomoe Shimazaki, Koji Yamamoto, Taku Shigesawa, Akihisa Nakamura, Masatsugu Ohara, Naoki Kawagishi, Masato Nakai, Takuya Sho, Mitsuteru Natsuizaka, Kenichi Morikawa, Koji Ogawa, Naoya Sakamoto

    Hepatology research : the official journal of the Japan Society of Hepatology   49 ( 11 )   1294 - 1304   2019.11

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    AIM: Entecavir (ETV), tenofovir disoproxil fumarate (TDF), and tenofovir alafenamide (TAF) are first-line nucleos(t)ide analogues for hepatitis B virus (HBV)-infected patients. However, consecutive TDF treatment causes renal dysfunction, and the safety and efficacy of TAF have not been established in severe renal dysfunction patients, including hemodialysis patients. The efficacy and safety of ETV in these populations has not been clarified. The study aimed to clarify this. METHODS: In this retrospective multicenter study, between 2006 and 2018, a total of 567 HBV-infected patients treated with ETV monotherapy were screened. Patients were included if >20 years old, treated with ETV monotherapy for >1 year, and had proper clinical information. The efficacy of ETV and changes in renal function were evaluated according to renal function. RESULTS: A total of 273 patients were included: 9.2% (25/273), 1.8% (5/273), and 3.7% (10/273) had chronic kidney disease (CKD) stage G3, CKD stage G4/5, and were on hemodialysis, respectively. Overall, 84.2%, 94.0%, and 96.2% of patients experienced serum HBV-DNA disappearance at 1, 2, and 3 years, respectively, after treatment initiation. In patients with CKD stage G3-5, estimated glomerular filtration rate tended to restore with time, which was in contrast to patients without renal dysfunction. The rate of disappearance in serum HBV-DNA, alanine transaminase normalization, and virological breakthrough was similar between patients with or without renal dysfunction. ETV showed high efficacy for all 10 hemodialysis patients without virological breakthrough. CONCLUSIONS: Entecavir for HBV-infected patients with severe renal dysfunction, including hemodialysis patients, is highly effective and does not affect renal function.

    DOI： 10.1111/hepr.13399

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  • Extracellular vesicles from amnion-derived mesenchymal stem cells ameliorate hepatic inflammation and fibrosis in rats. Reviewed

    Ohara M, Ohnishi S, Hosono H, Yamamoto K, Yuyama K, Nakamura H, Fu Q, Maehara O, Suda G, Sakamoto N.

    Stem Cells International.   2018.12

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  • Effects of human amnion-derived mesenchymal stem cells and conditioned medium in rats with sclerosing cholangitis. Reviewed

    Sugiura R, Ohnishi S, Ohara M, Ishikawa M, Miyamoto S, Onishi R, Yamamoto K, Kawakubo K, Kuwatani M, Sakamoto N.

    Am J Transl Res.   2018.7

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  • Palmitoylethanolamide ameliorates carbon tetrachloride-induced liver fibrosis in rats. Reviewed

    Ohara M, Ohnishi S, Hosono H, Yamamoto K, Fu Q, Maehara O, Suda G, Sakamoto N.

    Front Pharmacol.   2018.7

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  • Extracellular vesicles from amnion-derived mesenchymal stem cells ameliorate hepatic inflammation and fibrosis in rats. Reviewed International journal

    Ohara M, Ohnishi S, Hosono H, Yamamoto K, Yuyama K, Nakamura H, Fu Q, Maehara O, Suda G, Sakamoto N

    Stem Cells International (in press)   2018   3212643 - 3212643   2018

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    Background: There are no approved drug treatments for liver fibrosis and nonalcoholic steatohepatitis (NASH), an advanced stage of fibrosis which has rapidly become a major cause of cirrhosis. Therefore, development of anti-inflammatory and antifibrotic therapies is desired. Mesenchymal stem cell- (MSC-) based therapy, which has been extensively investigated in regenerative medicine for various organs, can reportedly achieve therapeutic effect in NASH via paracrine action. Extracellular vesicles (EVs) encompass a variety of vesicles released by cells that fulfill functions similar to those of MSCs. We herein investigated the therapeutic effects of EVs from amnion-derived MSCs (AMSCs) in rats with NASH and liver fibrosis. Methods: NASH was induced by a 4-week high-fat diet (HFD), and liver fibrosis was induced by intraperitoneal injection of 2 mL/kg 50% carbon tetrachloride (CCl4) twice a week for six weeks. AMSC-EVs were intravenously injected at weeks 3 and 4 in rats with NASH (15 μg/kg) and at week 3 in rats with liver fibrosis (20 μg/kg). The extent of inflammation and fibrosis was evaluated with quantitative reverse transcription polymerase chain reaction and immunohistochemistry. The effect of AMSC-EVs on inflammatory and fibrogenic response was investigated in vitro. Results: AMSC-EVs significantly decreased the number of Kupffer cells (KCs) in the liver of rats with NASH and the mRNA expression levels of inflammatory cytokines such as tumor necrosis factor- (Tnf-) α, interleukin- (Il-) 1β and Il-6, and transforming growth factor- (Tgf-) β. Furthermore, AMSC-EVs significantly decreased fiber accumulation, KC number, and hepatic stellate cell (HSC) activation in rats with liver fibrosis. In vitro, AMSC-EVs significantly inhibited KC and HSC activation and suppressed the lipopolysaccharide (LPS)/toll-like receptor 4 (TLR4) signaling pathway. Conclusions: AMSC-EVs ameliorated inflammation and fibrogenesis in a rat model of NASH and liver fibrosis, potentially by attenuating HSC and KC activation. AMSC-EV administration should be considered as a new therapeutic strategy for chronic liver disease.

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  • Palmitoylethanolamide Ameliorates Carbon Tetrachloride-Induced Liver Fibrosis in Rats. Reviewed International journal

    Ohara M, Ohnishi S, Hosono H, Yamamoto K, Fu Q, Maehara O, Suda G, Sakamoto N

    Frontiers in pharmacology   9   709 - 709   2018

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    Background: Liver fibrosis is a complex inflammatory and fibrogenic process, and the progression of fibrosis leads to cirrhosis. The only therapeutic approaches are the removal of injurious stimuli and liver transplantation. Therefore, the development of anti-fibrotic therapies is desired. Palmitoylethanolamide (PEA) is an endogenous fatty acid amide belonging to the N-acylethanolamines family and contained in foods such as egg yolks and peanuts. PEA has therapeutic anti-inflammatory, analgesic, and neuroprotective effects. However, the effects and roles of PEA in liver fibrosis remain unknown. Here we investigated the therapeutic effects of PEA in rats with liver fibrosis. Methods: We conducted in vitro experiments to investigate the effects of PEA on the activation of hepatic stellate cells (HSCs, LX-2). Liver fibrosis was induced by an intraperitoneal injection of 1.5 mL/kg of 50% carbon tetrachloride twice a week for 4 weeks. Beginning at 3 weeks, PEA (20 mg/kg) was intraperitoneally injected thrice a week for 2 weeks. Then rats were sacrificed and we performed histological and quantitative reverse-transcription polymerase chain reaction analyses. Results: The expression of α-smooth muscle actin (SMA) induced by transforming growth factor (TGF)-β1 in HSCs was significantly downregulated by PEA. PEA treatment inhibited the TGF-β1-induced phosphorylation of SMAD2 in a dose-dependent manner, and upregulated the expression of SMAD7. The reporter gene assay demonstrated that PEA downregulated the transcriptional activity of the SMAD complex upregulated by TGF-β1. Administration of PEA significantly reduced the fibrotic area, deposition of type I collagen, and activation of HSCs and Kupffer cells in rats with liver fibrosis. Conclusion: Activation of HSCs was significantly decreased by PEA through suppression of the TGF-β1/SMAD signaling pathway. Administration of PEA produced significant improvement in a rat model of liver fibrosis, possibly by inhibiting the activation of HSCs and Kupffer cells. PEA may be a potential new treatment for liver fibrosis.

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  • Effects of human amnion-derived mesenchymal stem cells and conditioned medium in rats with sclerosing cholangitis. Reviewed International journal

    Sugiura R, Ohnishi S, Ohara M, Ishikawa M, Miyamoto S, Onishi R, Yamamoto K, Kawakubo K, Kuwatani M, Sakamoto N

    American journal of translational research   10 ( 7 )   2102 - 2114   2018

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  • Genetic variants of Helicobacter pylori type IV secretion system components CagL and CagI and their association with clinical outcomes. Reviewed

    Ogawa H, Iwamoto A, Tanahashi T, Okada R, Yamamoto K, Nishiumi S, Yoshida M, Azuma T.

    Gut pathogens   2017.4

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  • Genetic variants of Helicobacter pylori type IV secretion system components CagL and CagI and their association with clinical outcomes Reviewed International journal

    Hirofumi Ogawa, Akira Iwamoto, Toshihito Tanahashi, Rina Okada, Koji Yamamoto, Shin Nishiumi, Masaru Yoshida, Takeshi Azuma

    GUT PATHOGENS   9   21 - 21   2017.4

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    DOI： 10.1186/s13099-017-0165-1

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection. Reviewed

    Yang L, Yamamoto K (equally first author), Nishiumi S, Nakamura M, Matsui M, Takahashi S, Dohi T, Okada T, Kakimoto K, Hoshi N, Yoshida M, Azuma T.

    Mucosal Immunology   2015.3

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  • Interferon-gamma-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection Reviewed

    L. Yang, K. Yamamoto, S. Nishiumi, M. Nakamura, H. Matsui, S. Takahashi, T. Dohi, T. Okada, K. Kakimoto, N. Hoshi, M. Yoshida, T. Azuma

    MUCOSAL IMMUNOLOGY   8 ( 2 )   279 - 295   2015.3

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    DOI： 10.1038/mi.2014.66

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  • 抗CXCL13抗体は、Helicobacter suis感染によって誘導された胃リンパ濾胞形成を抑制する Invited Reviewed

    山本幸司, 吉田優, Azuma Takeshi

    日本ヘリコバクター学会誌   16 ( 2号 )   4 - 9   2015.1

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  • Anti-CXCL13 antibody can inhibit the formation of gastric lymphoid follicles induced by Helicobacter infection Reviewed

    K. Yamamoto, S. Nishiumi, L. Yang, E. Klimatcheva, T. Pandina, S. Takahashi, H. Matsui, M. Nakamura, M. Zauderer, M. Yoshida, T. Azuma

    MUCOSAL IMMUNOLOGY   7 ( 5 )   1244 - 1254   2014.9

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    DOI： 10.1038/mi.2014.14

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  • Anti-CXCL13 antibody can inhibit the formation of gastric lymphoid follicles induced by Helicobacter infection. Reviewed

    Yamamoto K, Nishiumi S, Yang L, Klimatcheva E, Pandina T, Takahashi S, Matsui H, Nakamura M, Zauderer M, Yoshida M, Azuma T.

    Mucosal Immunology   2014.7

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  • Whole-genome sequencing of clarithromycin resistant Helicobacter pylori characterizes unidentified variants of multidrug resistant efflux pump genes Reviewed International journal

    Akira Iwamoto, Toshihito Tanahashi, Rina Okada, Yukio Yoshida, Kaoru Kikuchi, Yoshihide Keida, Yoshiki Murakami, Lin Yang, Koji Yamamoto, Shin Nishiumi, Masaru Yoshida, Takeshi Azuma

    GUT PATHOGENS   6   27 - 27   2014.6

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    DOI： 10.1186/1757-4749-6-27

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  • Whole-genome sequencing of clarithromycin resistant Helicobacter pylori characterizes unidentified variants of multidrug resistant efflux pump genes. Reviewed

    Iwamoto A, Tanahash T, Okada R, Yoshida Y, Kikuchi K, Keida Y, Murakami Y, Yang L, Yamamoto K, Nishiumi S, Yoshida M and Azuma T.

    Gut pathogens   2014.1

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  • Intestinal anti-inflammatory activity of luteolin: role of the aglycone in NF-kappa B inactivation in macrophages co-cultured with intestinal epithelial cells Reviewed International journal

    Yosuke Nishitani, Koji Yamamoto, Masaru Yoshida, Takeshi Azuma, Kazuki Kanazawa, Takashi Hashimoto, Masashi Mizuno

    BIOFACTORS   39 ( 5 )   522 - 533   2013.9

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    DOI： 10.1002/biof.1091

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  • Intestinal anti-inflammatory activity of luteolin: role of the aglycone in NF-B inactivation in macrophages co-cultured with intestinal epithelial cells. Reviewed

    Nishitani Y, Yamamoto K, Yoshida M, Azuma T, Kanazawa K, Hashimoto T and Mizuno M.

    Biofactors   2013.3

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  • Autophagy in the intestinal epithelium regulates Citrobacter rodentium infection Reviewed

    Jun Inoue, Shin Nishiumi, Yoshimi Fujishima, Atsuhiro Masuda, Hideyuki Shiomi, Koji Yamamoto, Masayuki Nishida, Takeshi Azuma, Masaru Yoshida

    ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS   521 ( 1-2 )   95 - 101   2012.5

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    DOI： 10.1016/j.abb.2012.03.019

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  • Autophagy in the intestinal epithelium regulates Citrobacter rodentium infection. Reviewed

    Inoue J, Nishiumi S, Fujishima Y, Masuda A, Shiomi H, Yamamoto K, Nishida M, Azuma T, Yoshida M.

    Arch Biochem Biophys   2012.3

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  • Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice. Reviewed

    Slayman YB, Yoshida M, Nishiumi S, Tanaka H, Mimura T, Nobutani K, Yamamoto K, Takenaka M, Ota H, Takahashi S, Matsui H, Nakamura M, Blumberg RS, Azuma T.

    Mucosal Immunology   2012.1

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  • Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice Reviewed

    Y. Ben Suleiman, M. Yoshida, S. Nishiumi, H. Tanaka, T. Mimura, K. Nobutani, K. Yamamoto, M. Takenaka, A. Aoganghua, I. Miki, H. Ota, S. Takahashi, H. Matsui, M. Nakamura, R. S. Blumberg, T. Azuma

    MUCOSAL IMMUNOLOGY   5 ( 1 )   87 - 98   2012.1

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    DOI： 10.1038/mi.2011.53

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  • IFN-gamma plays an essential role in the pathogenesis of gastric lymphoid follicles formation caused by Helicobacter suis infection Reviewed International journal

    Takuya Mimura, Masaru Yoshida, Shin Nishiumi, Hiroshi Tanaka, Kentaro Nobutani, Mamoru Takenaka, Yahaya Ben Suleiman, Koji Yamamoto, Hiroyoshi Ota, Shinichi Takahashi, Hidenori Matsui, Masahiko Nakamura, Ikuya Miki, Takeshi Azuma

    FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY   63 ( 1 )   25 - 34   2011.10

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    DOI： 10.1111/j.1574-695X.2011.00823.x

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  • IFN-γ plays an essential role in the pathogenesis of gastric lymphoid follicles formation caused by Helicobacter suis infection. Reviewed

    Mimura T, Yoshida M, Nishiumi S, Tanaka H, Nobutani K, Takenaka M, Slayman YB, Yamamoto K, Ota H, Takahashi S, Matsui H, Nakamura M, Miki I, Azuma T.

    FEMS Immunol Med Microbiol.   2011.7

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  • Helicobacter suis KB1 derived from pig gastric lymphoid follicles induces the formation of gastric lymphoid follicles in mice through the activation of B cells and CD4 positive cells Reviewed International journal

    Koji Yamamoto, Hiroshi Tanaka, Yosuke Nishitani, Shin Nishiumi, Ikuya Miki, Mamoru Takenaka, Kentaro Nobutani, Takuya Mimura, Yahaya Ben Suleiman, Shigeto Mizuno, Mikihiko Kawai, Ikuo Uchiyama, Masaru Yoshida, Takeshi Azuma

    MICROBES AND INFECTION   13 ( 7 )   697 - 708   2011.7

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    DOI： 10.1016/j.micinf.2011.02.007

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  • Helicobacter suis KB1 derived from pig gastric lymphoid follicles induces the formation of gastric lymphoid follicles in mice through the activation of B cells and CD4 positive cells. Reviewed

    Yamamoto K, Tanaka H, Nishitani Y, Nishiumi S, Miki Y, Takenaka M, Nobutani K, Mimura T, Yahaya Ben Suleiman, Mizuno S, Kawai M, Uchiyama I, Yoshida M, Azuma T.

    Microbes Infect.   2011.3

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  • Helicobacter heilmannii can induce gastric lymphoid follicles in mice via a Peyer&apos;s patch-independent pathway Reviewed International journal

    Kentaro Nobutani, Masaru Yoshida, Shin Nishiumi, Yosuke Nishitani, Tetsuya Takagawa, Hiroshi Tanaka, Koji Yamamoto, Takuya Mimura, Yahaya Bensuleiman, Hiroyoshi Ota, Shinichi Takahashi, Hidenori Matsui, Masahiko Nakamura, Takeshi Azuma

    FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY   60 ( 2 )   156 - 164   2010.11

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    DOI： 10.1111/j.1574-695X.2010.00731.x

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  • Helicobacter heilmannii can induce gastric lymphoid follicles in mice via a Peyer's patch-independent pathway. Reviewed

    Nobutani K, Yoshida M, Nishiumi S, Nishitani Y, Takagawa T, Tanaka H, Yamamoto K, Mimura T, Bensuleiman Y, Ota H, Takahashi S, Matsui H, Nakamura M, Azuma T.

    FEMS Immunol Med Microbiol.   2010.9

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  • The CagA protein of Helicobacter pylori suppresses the functions of dendritic cell in mice Reviewed International journal

    Hiroshi Tanaka, Masaru Yoshida, Shin Nishiumi, Naomi Ohnishi, Kazuki Kobayashi, Koji Yamamoto, Tsuyoshi Fujita, Masanori Hatakeyama, Takeshi Azuma

    ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS   498 ( 1 )   35 - 42   2010.6

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    DOI： 10.1016/j.abb.2010.03.021

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  • Monoacetylcurcumin strongly regulates inflammatory responses through inhibition of NF-kappa B activation Reviewed International journal

    Masayuki Nishida, Shin Nishiumi, Yoshiyuki Mizushina, Yoshimi Fujishima, Koji Yamamoto, Atsuhiro Masuda, Shigeto Mizuno, Tsuyoshi Fujita, Yoshinori Morita, Hiromu Kutsumi, Hiromi Yoshida, Takeshi Azuma, Masaru Yoshida

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE   25 ( 5 )   761 - 767   2010.5

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    DOI： 10.3892/ijmm_00000402

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  • The CagA protein of Helicobacter pylori suppresses the functions of dendritic cell in mice. Reviewed

    Tanaka H, Yoshida M, Nishiumi S, Ohnishi N, Kobayashi K, Yamamoto K, Fujita T, Hatakeyama M, Azuma T.

    Arch Biochem Biophys   2010.4

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  • Monoacetylcurcumin regulates anti-inflammatory activity through inhibition of NF-kB activation. Reviewed

    Nishida M, Nishiumi S, Mizushina Y, Fujishima Y, Yamamoto K, Masuda A, Mizuno S, Fujita T, Morita Y, Kutsumi H, Azuma T, and Yoshida M.

    Int J Mol Med.   2010.1

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  • Epstein-Barr virus BZLF1 gene, a switch from latency to lytic infection, is expressed as an immediate-early gene after primary infection of B lymphocytes. Reviewed

    Wen W, Iwakiri D, Yamamoto K, Maruo S, Kanda T, Takada K.

    J Virol.   2007.1

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  • Epstein-Barr virus BZLF1 gene, a switch from latency to lytic infection, is expressed as an immediate-early gene after primary infection of B lymphocytes Reviewed International journal

    Wangrong Wen, Dal Iwakiri, Koji Yamamoto, Seiji Maruo, Teru Kanda, Kenzo Takada

    JOURNAL OF VIROLOGY   81 ( 2 )   1037 - 1042   2007.1

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    DOI： 10.1128/JVI.01416-06

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Books

  • メタゲノム解析技術の最前線, 疾患とメタゲノム (腸内細菌と炎症性腸疾患)

    山本　幸司, 吉田　優, 井上　潤, 大井 充, 吉江　智郎, 東　健.（ Role： Joint author）

    シーエムシー出版  2017.2 

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MISC

  • OLEOYLETHANOLAMIDE AMELIORATES DEXTRAN SULFATE SODIUM-INDUCED COLITIS IN RATS

    Shinsuke Otagiri, Shunsuke Ohnishi, Masatsugu Ohara, Qingjie Fu, Koji Yamamoto, Takehiko Katsurada, Naoya Sakamoto

    GASTROENTEROLOGY   158 ( 6 )   S275 - S275   2020.5

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  • ヒト羊膜由来間葉系幹細胞を用いた再生医療研究

    山本　幸司, 大西　俊介

    遺伝子医学   2019.4

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  • 羊膜間葉系幹細胞由来細胞外小胞の慢性肝障害モデルに対する抗炎症・抗線維化効果

    大原正嗣, 大西俊介, 山本幸司, 付慶傑, 前原経, 須田剛生, 坂本直哉

    日本再生医療学会総会(Web)   18th   2019

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Presentations

  • Identification of Macrophages Directly Associated with the Onset of Metaboli c Dysfunction Associated Steatohepatitis

    Koji Yamamoto, Masatomo, Takahasi, Yoshihiro Izumi

    2025.11 

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  • Effects of Trimethylamine N-oxide on Cardiomyocytes in Heart Failure Formation

    APPW2025  2025.3 

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  • Identification of Macrophage Directly Associated with the Onset of Non-Alcoholic Steatohepatitis (NASH)

    Koji Yamamoto, Yumiko Chiba, Toshiyuki Kaneko, Gentaro Iribe

    APPW2025  2025.3 

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  • Myocardial stretch-induced ROS production was increased via inter-organ network

    APPW2025  2025.3 

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  • 非アルコール性脂肪肝炎（NASH）の発症に直接的に関連するマクロファージの同定

    山本 幸司, 千葉 弓子, 金子 智之, 入部玄太郎

    第１０４回北海道医学大会生理系分科会  2024.9 

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  • Tolvaptan as an alternative treatment for refractory fluid retention associated with sinusoidal obstruction syndrome after allogeneic stem cell transplantation Invited International conference

    Yakushijin Kimikazu, Kurata K, Miyata T, Kakiuchi S, Tomioka H, Kawamori-Iwamoto Y, Inui Y, Sanada Y, Okamura A, Yamamoto Koji, Murayama T, Matsuoka H, Minami Hironobu

    The 17th meeting of Asia Pacific Blood and Marrow Transplantation Group  2012.10  Asia Pacific Blood and Marrow Transplantation Group

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    Venue：India  

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  • Prospective observational study on chemotherapy-induced nausea and vomiting (CINV) for hepatobiliary and pancreatic cancer patients who were to receive chemotherapy including cisplatin by the CINV study group of Japan. Invited International conference

    Furuse J, Baba Hisamitsu, Ohkawa S, Sugimori K, Yamamoto Koji, Minami Hironobu, Kitagawa Y, Kuramochi H, Kwon A, Unno M, Wakabayashi G, Aiba K, Tamura K

    Gastrointestinal Cancers Symposium  2015.1  ASCO

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    Venue：San Francisco, アメリカ  

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  • Anti-CXCL13 antibody can inhibit the formation of gastric lymphoid follicles induced by Helicobacter infection. Invited International conference

    Yamamoto Koji, Lin Yang, Azuma Takeshi

    The 5th International Symposium on Carcinogenic Infection, Immunity, and Cancer  2015.2  Infection/Inflammation-Assisted Acceleration of the Carcinogenic Spiral and Its Alteration though vector Conversion of the Host Response to Tumors Scientific Research on Innovative Areas, a MEXT Grant-in-Aid Project

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    Venue：神戸  

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection. Invited

    Lin Yang, Yamamoto Koji, Azuma Takeshi

    The 5th International Symposium on Carcinogenic Infection, Immunity, and Cancer  2015.2  Infection/Inflammation-Assisted Acceleration of the Carcinogenic Spiral and Its Alteration though vector Conversion of the Host Response to Tumors Scientific Research on Innovative Areas, a MEXT Grant-in-Aid Project

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    Venue：神戸  

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  • Anti-CXCL13 antibody can inhibit the formation of gastric lymphoid follicles induced by Helicobacter infection. Invited

    Yamamoto Koji

    The 88th Annual Meeting of Japanese Society for Bacteriology  2015.3  apanese Society for Bacteriology

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    Venue：滋賀  

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  • インターフェロン産生B細胞は、H. suis感染後の胃リンパ濾胞形成を誘導する。 Invited

    Yamamoto Koji, Azuma Takeshi

    第21回日本ヘリコバクター学会学術集会  2015.6 

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    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：神戸  

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  • Whole-genome sequencing detects novel missense variants of Helicobacter pylori cagA gene related to the oncogenic CagA Invited

    岩本 彰, 棚橋 俊仁, 小川 浩史, 楊 林, Yamamoto Koji, Azuma Takeshi

    第21回日本ヘリコバクター学会学術集会  2015.6 

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    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：神戸  

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  • インターフェロン産生B細胞は、H. suis感染後の胃リンパ濾胞形成を誘導する。 Invited

    Yamamoto Koji, Azuma Takeshi

    第80回日本インターフェロン・サイトカイン学会  2015.7 

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：東京  

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  • A case of myeloid sarcoma with myelofibrosis secondary to polycthemia vera

    Ohmiya S, Kurata K, Nose T, Kawamoto Teruya, Kawamoto Shinichiro, Yakushijin Kimikazu, Yamamoto Koji, Ito T, Matsuoka Hiroshi, Minami Hironobu

    第77回日本血液学会学術集会  2015.10 

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    Language：English   Presentation type：Poster presentation  

    Venue：金沢  

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  • A case of scopulariopsis pneumonia with acute myeloid leukemia

    Kim S, Kurata K, Yokoro Y, Goto H, Mizutani Y, Takenaka K, Otera Hiroshi, Kawamoto Shinichiro, Yakushijin Kimikazu, Yamamoto Koji, Ito T, Matsuoka Hiroshi, Minami Hironobu

    第77回日本血液学会学術集会  2015.10 

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    Language：English   Presentation type：Poster presentation  

    Venue：金沢  

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection. Invited

    Yamamoto Koji, Azuma Takeshi

    第68回日本細菌学会関西支部総会  2015.11 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：京都  

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  • Anti-CXCL13 antibody can inhibit against the formation of gastric lymphoid follicles induced by Helicobacter infection Invited

    Yamamoto Koji, Azuma Takeshi

    第38回日本分子生物学会、第88回日本生化学会合同大会  2015.12 

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    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：神戸  

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  • Retrospective analysis of safety and efficacy of (R-) LEED and (R-) MCEC regimens followed by autologous peripheral blood stem cell transplantation for non-Hodgkin&apos;s lymphoma. Invited International conference

    Miyata T, Tominaga R, Gomyo R, Maeda A, Mizuno I, Yakushijin Kimikazu, Okamura A, Yamamoto Koji, Matsuoka H, Minami Hironobu, Murayama T

    The 17th meeting of Asia Pacific Blood and Marrow Transplantation Group  2012.10  Asia Pacific Blood and Marrow Transplantation Group

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    Language：English   Presentation type：Poster presentation  

    Venue：India  

    Retrospective analysis of safety and efficacy of (R-) LEED and (R-) MCEC regimens followed by autologous peripheral blood stem cell transplantation for non-Hodgkin&apos;s lymphoma.

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection. Invited

    Yamamoto Koji, Lin Yang, Azuma Takeshi

    The 87th Annual Meeting of the Japanese Sociaty of the Japanese Biochemical Sociaty  2014.10  the Japanese Sociaty of the Japanese Biochemical Sociaty

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    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：京都  

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection. International conference

    Lin Yang, Yamamoto Koji, Azuma Takeshi

    University of Washington and Kobe University International Joint Symposium  2014.12  Kobe University Graduate School of Medicine

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    Language：English   Presentation type：Poster presentation  

    Venue：神戸  

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  • 萎縮性胃炎に関与するヘリコバクターピロリ菌のCagA分子多型とクラリスロマイシン耐性に関わる全ゲノム変化の解析 Invited

    岩本 彰, 棚橋 俊仁, 岡田 理菜, 吉田 幸生, 菊地 馨, 慶田 喜秀, 村上 善基, 楊 林, Yamamoto Koji, Nishiumi Sin, Yoshida Masaru, Azuma Takeshi

    第10回日本消化管学会総会学術集会  2014.2  日本消化管学会

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    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：福島  

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  • Anti-CXCL13 antibody can inhibit the formation of gastric lymphoid follicles induced by Helicobacter infection. Invited International conference

    Yamamoto Koji, Azuma Takeshi

    The 20th Annual Meeting of the Japanese Sociaty of Helicobacter Research  2014.6  The Japanese Sociaty of Helicobacter Research

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    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：東京  

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  • Anti-CXCL13 antibody can inhibit the formation of gastric lymphoid follicles induced by Helicobacter infection. Invited

    Yamamoto Koji, Azuma Takeshi

    The 79th Annual Meeting of the Japanese Sociaty of Interferon & Cytokine Research  2014.6  The Japanese Sociaty of Interferon & Cytokine Research

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：札幌  

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection. Invited

    Lin Yang, Yamamoto Koji, Azuma Takeshi

    The 20th Annual Meeting of the Japanese Sociaty of Helicobacter Research  2014.6  The Japanese Sociaty of Helicobacter Research

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    Language：English   Presentation type：Poster presentation  

    Venue：東京  

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  • Characterization of full sequences of Japanese H. pylori cagA gene using next-generation sequencing Invited

    岩本 彰, 棚橋 俊仁, 楊 林, Yamamoto Koji, Azuma Takeshi

    第20回ヘリコバクター学会学術集会  2014.6  日本ヘリコバクター学会

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    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：東京  

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection.

    Lin Yang, Yamamoto Koji, Azuma Takeshi

    The 2nd ShinryokukaiYoung Investigator Award Presentation Meeting  2014.10  Kobe University Graduate School of Medicine

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    Language：English   Presentation type：Poster presentation  

    Venue：神戸  

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  • Anti-CXCL13 antibody can protect against gastric lymphoid follicles induced by Helicobacter infection Invited

    楊 林, Yamamoto Koji, Azuma Takeshi

    第19回日本ヘリコバクター学会学術集会  2013.6  日本ヘリコバクター学会

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    Language：English   Presentation type：Oral presentation (general)  

    Venue：長崎  

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection Invited

    楊 林, Yamamoto Koji, Azuma Takeshi

    「がん研究分野の特性等を踏まえた支援活動」 公開シンポジウム  2014.1  文部科学省 新学術領域研究

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    Language：English   Presentation type：Poster presentation  

    Venue：東京  

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  • Anti-CXCL13 antibody can protect against gastric lymphoid follicles induced by Helicobacter infection Invited

    Yamamoto Koji, 楊 林, Azuma Takeshi

    第4回新学術領域発がんスパイラル国際シンポジウム  2014.2  文部科学省科研費 新学術領域「発がんスパイラル」

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：札幌  

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection Invited

    楊 林, Yamamoto Koji, Azuma Takeshi

    第4回新学術領域発がんスパイラル国際シンポジウム  2014.2  文部科学省科研費 新学術領域「発がんスパイラル」

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    Language：English   Presentation type：Poster presentation  

    Venue：札幌  

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  • Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection. Invited

    Yamamoto Koji, Azuma Takeshi

    第89回日本細菌学会総会  2016.3 

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    Language：Japanese   Presentation type：Poster presentation  

    Venue：大阪  

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  • Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates the bacterial infection in mice. Invited

    ヤハヤ ベンスレイマン, Yoshida Masaru, 田中 擴址, Yamamoto Koji

    第16回日本ヘリコバクター学会  2010.6  日本ヘリコバクター学会

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    Language：English   Presentation type：Poster presentation  

    Venue：京都  

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  • Candica parapsilosis as a cause for rhabdomyolysis in a patient with acute myeloid leukemia after bone marrow transplantation. Invited International conference

    Kakiuchi S, Yakushijin Kimikazu, Tomioka H, Kawamori-Iwamoto Y, Inui Y, Okamura A, Yamamoto Koji, Murayama T, Matsuoka H, Minami Hironobu

    The 17th meeting of Asia Pacific Blood and Marrow Transplantation Group  2012.10  Asia Pacific Blood and Marrow Transplantation Group

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    Language：English   Presentation type：Poster presentation  

    Venue：India  

    Candica parapsilosis as a cause for rhabdomyolysis in a patient with acute myeloid leukemia after bone marrow transplantation.

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Industrial property rights

  • 抗炎症作用を有する細胞外小胞製剤

    林 真広, 中石 智之, 大西 俊介, 山本 幸司, 武井 則雄, 大久保 直登

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    Application no：特願2022-073684  Date applied：2022.4

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  • METHODS FOR INCREASING IMMUNOGLOBULIN A LEVELS

    Masaru Yoshida, Koji Yamamoto, Maurice Zauderer and Ernest S. Smith.

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    Application no：US2014/014107  Date applied：2015.12

    Country of applicant：International (PCT) application  

  • METHODS FOR INCREASING IMMUNOGLOBULIN A LEVELS

    Masaru Yoshida (JP, Koji Yamamoto (J., Maurice Zauderer, Ernest S. Smith

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    Application no：特願US 2015/0368332 A1  Date applied：2015.12

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Awards

  • 第４回神緑会Young Investigator Award　優秀賞

    2016.10   一般社団法人神緑会  

    山本幸司

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    Country：Japan

  • 第4回神緑会Young Investigator Award 優秀賞

    2016.10  

    山本 幸司

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  • 第68回日本細菌学会関西支部総会　若手研究者奨励賞

    2015.11   日本細菌学会  

    山本幸司

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    Award type：Award from Japanese society, conference, symposium, etc.  Country：Japan

  • 第68回日本細菌学会関西支部総会 若手研究者奨励賞

    2015.11   第68回日本細菌学会関西支部   学部学生、大学院生、および 40 歳未満（支部総会当日）の若手研究者

    Yamamoto Koji

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    Award type：Award from Japanese society, conference, symposium, etc. 

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  • 第20回日本ヘリコバクター学会 上原H. pylori最優秀賞

    2014.6   日本ヘリコバクター学会  

    山本幸司

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    Award type：Award from Japanese society, conference, symposium, etc.  Country：Japan

  • 上原H. pylori最優秀賞

    2014.6   日本ヘリコバクター学会会員

    Yamamoto Koji

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    Award type：Award from Japanese society, conference, symposium, etc. 

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Research Projects

  • Investigation of the NASH-Suppressing Effects Targeting a Novel Metabolite That Induces Abnormalization of Liver Macrophages

    Grant number：25K14859  2025.4 - 2028.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Grant amount：\4,550,000 （ Direct Cost: \3,500,000 、 Indirect Cost：\1,050,000 ）

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  • 羊膜MSC由来HSPB6陽性エクソソームを用いた炎症性腸疾患への治療効果の検討

    2021.4 - 2024.3

    基盤研究(C)

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    これまでに我々は、複数の炎症性疾患動物モデルを用いて羊膜MSCの病態改善効果を明らかにしてきた。しかしながら、これまで羊膜MSCに由来するどのような物質がさまざまな炎症性疾患の病態を改善しているのかの詳細は明らかにされていない。本研究では、羊膜MSCから多量に産生されるHSPB6陽性エクソソームならびにHSPB6欠損エクソソームを樹立し、それらエクソソームを用いた抗炎症効果の詳細を細胞実験ならびに炎症性腸疾患誘導性動物モデルを用いて検証する。これらの検証実験を踏まえ未だ適切な治療法がないヒト炎症性腸疾患に対する臨床応用への基盤を整える。

  • Examination of the therapeutic effect on inflammatory bowel disease using HSPB6-positive exosomes derived from amnion-derived MSCs

    Grant number：21K07952  2021.4 - 2024.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Grant amount：\4,030,000 （ Direct Cost: \3,100,000 、 Indirect Cost：\930,000 ）

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  • DSS誘発大腸炎モデル動物および乳房再建モデル動物、顔面神経麻痺モデル動物を用いた羊膜MSCの有効性評価と膵炎治療用デバイスの開発

    2021.4 - 2022.3

    株式会社 カネカ 

  • Identification of novel anti-inflammatory factor secreted by amnion-derived mesenchymal stem cells and investigation of therapeutic effect

    Grant number：20K08347  2020.4 - 2023.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Grant amount：\4,290,000 （ Direct Cost: \3,300,000 、 Indirect Cost：\990,000 ）

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  • ヒト羊膜MSCが持つ新規抗炎症物質の同定ならびに治療効果の検討

    2020.4 - 2022.3

    基盤研究(C)

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    申請者らは、羊膜MSCが多くの疾患で抗炎症効果を示すことを明らかにしてきたが、そのカギとなる抗炎症物質の存在は明らかにしていない。そこで、本研究では、羊膜MSCから新たに抗炎症物質持つ候補物質を同定し、その抗炎症効果を細胞実験で明らかにした。また、腸炎マウスモデルを用いて、羊膜MSC由来新規物質を投与したところ、腸管における炎症性サイトカインの発現は低下していたが、炎症性細胞の浸潤や病理学的なスコアリングでは、有意な改善効果は認められなかった。これらのことから、羊膜MSC由来新規因子は、細胞実験では抗炎症効果を示す傾向にあったが、動物実験においては著しい腸炎発症抑制効果は認められなかった。

  • 免疫チェックポイント阻害剤を用いたH. suis感染胃リンパ腫抑制効果の検討

    2019.4 - 2022.3

    基盤研究(C)

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    ヘリコバクタースイス (H. suis)は、人畜共通感染症の原因菌であり、胃MALTリンパ腫形成に関与している。近年、免疫チェックポイント阻害薬の使用が抗腫瘍効果を発揮することが知られている。本研究では、H. suis感染胃MALTリンパ腫発症マウスモデルを用いて、免疫チェックポイント阻害剤を投与したところ、胃MALTリンパ腫形成が有意に低下していることが明らかとなった。今後、これまで明らかにされていない胃MALTリンパ腫形成と免疫チャックポイント関連遺伝子発現との関連性が明らかになるばかりでなく、ヒトMALTリンパ腫患者に対する免疫チャックポイント阻害剤の有用性が期待される。

  • Examination of the inhibitory effect of H. suis-infected gastric MALT lymphoma formation using an immune checkpoint inhibitor

    Grant number：19K07553  2019.4 - 2022.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Yamamoto Koji

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    Grant amount：\4,290,000 （ Direct Cost: \3,300,000 、 Indirect Cost：\990,000 ）

    Helicobacter suis (H. suis) is a causative agent of zoonotic infections and is implicated in gastric MALT lymphoma. Recently, the use of immune checkpoint inhibitors has been known to exert an antitumor effect. In this study, we found that treatment with an immune checkpoint inhibitor significantly reduced gastric MALT lymphoma formation in H. suis-infected mice. In the future, the relationship between gastric MALT lymphoma formation and immune chuck point-related gene expression will be clarified, and the utility of immune chuck point inhibitors for human MALT lymphoma patients is expected.

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  • 羊膜由来間葉系幹細胞がもつEPA-レゾルビン産生と早産予防効果の検討

    2018.4 - 2021.3

    基盤研究(C)

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    間葉系幹細胞（MSC）は、骨髄、脂肪などに存在する体性幹細胞であり、骨、軟骨、脂肪などに分化する多分化能を有し、再生医療における有望な細胞として注目されている。本研究では、羊膜MSCから分泌される液性因子の解析から、エイコサペンタエン酸の代謝産物であるレゾルビンE1を同定した。また、LPS誘発早産ラットモデルに対してEPAを投与したところ、早産が抑制され、羊水中のEPAならびにレゾルビンE1の濃度も回復していた。以上のことから、EPAがレゾルビンE1を介して早産を予防している可能性が示唆された。

  • Effect of EPA-resolvin secreted from amnion-derived mesenchymal stem cells on premature birth

    Grant number：18K09214  2018.4 - 2021.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Ohnishi Shunsuke

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    Grant amount：\4,420,000 （ Direct Cost: \3,400,000 、 Indirect Cost：\1,020,000 ）

    Mesenchymal stem cells have been reported to be a promising cell source in regenerative medicine. We analyzed secretory factors from amnion-derived mesenchymal stem cells, and identified eicosapentaenoic acid (EPA) and its metabolite resovlin E1 (RvE1).
    When we administered EPA to LPS-induced premature birth model rats, it improved premature birth, and the concentrations of EPA and RvE1 in amniotic fluid were recovered. These results suggest that EPA prevents preterm birth via RvE1.

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  • H. suis感染胃MALTリンパ腫形成に関わるCXCL13発現メカニズムの解明

    2017.4 - 2019.3

    若手研究(B)

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    ヘリコバクタースイス(H. suis)は、ヒト胃MALTリンパ腫発症に関与している細菌であり、感染マウスにおいては、その100%の確率で胃にMALTリンパ腫を発症することが知られている。近年、申請者は、H. suis感染胃MALTリンパ腫形成にはIFN-γならびにCXCL13の遺伝子が重要であることを示したが、それらの遺伝子発現との関連性を示すメカニズムは明らかにされていない。 申請者は、H. suis感染後の胃で高発現するIFN-γが濾胞性樹状細胞を刺激することでCXCL13が産生され、胃MALTリンパ腫を発症させていることを明らかにした。

  • H. suis感染胃MALTリンパ腫形成に関わるCXCL13発現メカニズムの解明

    2017.4 - 2019.3

    学術研究助成基金助成金/若手研究B 

    山本 幸司

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    Authorship：Principal investigator  Grant type：Competitive

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  • サイトカイン・ケモカイン産生を介したH. suis感染後に誘導される胃MALTリンパ腫形成メカニズム

    2016.4 - 2017.3

    民間財団等 

  • H. suis感染における胃MALTリンパ腫形成とTLR4シグナル活性化機構の解明

    2015.4 - 2017.3

    若手研究(B)

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    本研究で我々は、H. suis感染後の胃MALTリンパ腫形成は、TLR4-TRIFシグナル伝達経路の活性化によって引き起こされることを明らかにした。また、TLR4-TRIFシグナル伝達経路の活性化により誘導される1型IFNsは、感染胃粘膜B細胞を刺激する結果、B細胞からのIFN-γの産生を促進することで胃MALTリンパ腫発症に関与していることも明らかとなった。これらの研究成果によりH. suis感染から胃MALTリンパ腫発症に関わる分子メカニズムが明らかとなり、今後、これらの分子メカニズムを標的とした胃MALTリンパ腫形成における新規治療法の開発が期待される。

  • H. suis感染による胃MALTリンパ腫形成とTLR4シグナル活性化機構の解明

    2015.4 - 2017.3

    学術研究助成基金助成金／若手研究(B) 

    山本 幸司

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    Authorship：Principal investigator  Grant type：Competitive

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