Role of the bactericidal lectin in bacterial enterocolitis
| Project/Area Number |
25460547
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 抗菌レクチン / 細菌性腸炎 / サルモネラ / 腸内細菌叢 / 感染性腸炎 |
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| Outline of Final Research Achievements |
The bactericidal lectin RegIIIbeta is secreted from intestinal epithelial cells into gut lumen. Expression of RegIIIbeta is inducible because gut infection with enteropathogens such as Salmonella dramatically increases the RegIIIbeta expression via MyD88- and IL-22-dependent manners. Thus, RegIII lectin is believed to act an innate immune effector. In contrast, the role of RegIIIbeta in gut infection with enteropathogens remains unknown. To this end, we have employed Salmonella colitis model with streptomycin-pretreated mouse. In Salmonella colitis model, the inducible expression of RegIIIbeta promoted sustained Salmonella gut colonization, and caused delayed recovery of the colitis. Microbiota analysis showed that RegIIIbeta inhibits rapid regrowth of certain commensal bacteria. Collectively, the RegIIIbeta-expressing gut microbiota remained dysbiosis, and thereby delaying recovery of the colitis. Our data have revealed that RegIIIbeta plays a pivotal role in Salmonella colitis.
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Report
(4 results)
Research Products
(3 results)
