Role of T cell-independent production of intestinal IgA in Clostridioides difficile enteritis
Project/Area Number |
17K16231
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Infectious disease medicine
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Research Institution | Teikyo University |
Principal Investigator |
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Project Period (FY) |
2017-04-01 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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Keywords | Clostridioides difficile / トキシンB / BAFF / 免疫調整 / 病原性 / B細胞活性化因子 / B細胞活性化因子(BAFF) / クロストリジウムディフィシル / 粘膜免疫 / IgA |
Outline of Final Research Achievements |
This study showed that C. difficile and its components could not lead to the production of B-cell activating factors from the intestinal epithelium and monocytes/macrophages.On the other hand, toxin B, the main virulence factor of C. difficile coordinated with flagellin, one of components of flagellum from bacteria and lead the efficient production of inflammatory cytokines like CCL-20.In addition, toxin B acted on monocyte/macrophage lineage cells and increased the production of B-cell activating factor via the stimulation of interferon-gamma. This study proved that Toxin B could regulate the immune response as well as its traditional function of mucosal disruption and local inflammatory activity.
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Academic Significance and Societal Importance of the Research Achievements |
本研究により、Clostridioides difficileの病原因子として、最も重要と考えられているトキシンBに免疫反応を活性化する機能を有していることを新たに見出した。C. difficile感染症は院内感染の一つとして知られ、重篤になれば死に至る可能性のある疾患である一方で、再発も多く、治療にしばしば難渋する。病原性についてはいまだ不明な部分も多く、その結果コントロールが難しくなっているものと考えられている。今回、トキシンBの新たな機能を見出したが、この結果はC. difficileの病原性解明の一助になるものと考えられる。
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Report
(4 results)
Research Products
(22 results)