| Project/Area Number |
23591461
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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 |
膠原病・アレルギー・感染症内科学
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| Research Institution | Keio University (2013-2014)
University of Yamanashi (2011-2012) |
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Principal Investigator |
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| Research Collaborator |
AKIHIKO Yoshimura 慶應義塾大学, 医学部, 教授 (90182815)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | アレルギー / 粘膜免疫 / 食品 / 微生物 / 食物アレルギー / 腸管粘膜 / サイトカイン |
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| Outline of Final Research Achievements |
Intestinal microflora has been implicated in regulation of allergies evoked by type 2 immunity. Here, we demonstrate that intestinal microflora negatively regulates murine food allergy model induced by oral ovalbumin (OVA)/cholera toxin (CT) immunization through intestinal mucosa by suppressing cytokine production from group 2 innate lymphoid cells (ILC2) cells. At early phase of OVA/CT treatment, IL-5 and 13 are mostly produced from ILC2 cells in the small intestine of immunized mice in an IL-33 dependent manner. The intestinal bacteria stimulate Th17 and γδT cell development, and IL-17 as well as IL-22 from these cells suppress food allergy, ILC2 accumulation in the intestine in vivo, and IL-5 and IL-13 expression from isolated ILC2 in vitro. Moreover, IL-33 release from the intestine was suppressed by IL-17 administration in vivo. Our results suggest that allergic diseases mediated by type 2 immunity can be prevented by the microbiota-mediated intestinal IL-23/IL-17 activation.
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