Suppression of food allergy by modulating autophagy function
Project/Area Number |
25461584
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | University of Fukui |
Principal Investigator |
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Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 食物アレルギー / オートファジー / 動物モデル / 免疫学 / 経口免疫寛容 |
Outline of Final Research Achievements |
Background: Autophagy is a fundamental bulk degradation process of cellular components. Autophagy is also associated with immune response. Therefore we analyzed the role of autophagy in the pathophysiology of food allergy. Methods: Balb/c mice were sensitized with Ovalbumin(OVA)/Alum and then were repetitively challenged with OVA. The effects of autophagy inhibitor, 3-methyladenine (3-MA) on allergic symptoms, mucosal mast cell protease-1 (mmcp-1), and OVA-specific cytokine producing ability of mesentric lymph node(MLN)cells, and mRNA expression levels in intestines were analyzed. Results: 3-MA treatment suppressed allergic symptoms induced by OVA challenge. In vitro OVA-specific Th2 cytokine production by MLN cells purified from 3-MA-treated mice were decreased compared with those of non-treated mice. 3-MA decreased the elevation of serum mmcp-1 levels and the expression levels of Th2 cytokine mRNA in the intestines.
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Report
(4 results)
Research Products
(19 results)