| Project/Area Number |
15K19092
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | Kobe University |
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Principal Investigator |
YAMAMOTO KOJI 神戸大学, 医学研究科, 学術研究員 (70608322)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | H. suis / 胃MALTリンパ腫 / TLR4-TRIFシグナル伝達 / 1型IFNs産生 / 胃粘膜B細胞 / IFN-γ産生 / IFN-γ / モノホスホリルリピドA / 胃上皮細胞 / TLR4-TRIFシグナリング |
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| Outline of Final Research Achievements |
Helicobacter suis (H. suis)is zoonotic infection related bacterium, which can induce the gastric mucosa associated lymphoid tissue (MALT) lymphoma. Recently, we reported that the formation of gastric lymphoid follicles after H. suis infection is induced via the activation of interferon (IFN)-γ. However, the detailed mechanism that how the activation of IFN-γ is induced after H. suis infection remained unclear. Here, we revealed that the activation of TLR4-TRIF pathway after H. suis infection is related to the production of type1 IFNs from gastric epithelial cells after H. suis infection. In addition, the production of type1 IFNs interacted with type 1 IFN receptors on gastric B cells to secret IFN-γ and then the activation of IFN-γ is enhanced by the positive feedback regulation of IFN-γ in B cells. These results suggest that TLR4-TRIF-type 1 IFN-IFN-γ pathway is crucial for the development of gastric lymphoid follicles after H. suis infection.
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