| Project/Area Number |
21591281
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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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 | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KANEHIRO Arihiko 岡山大学, 大学院・医歯薬学総合研究科, 准教授 (20243503)
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| Research Collaborator |
ERWIN W gelfand National Jewish Health, Denver, CO, USA, Department of Pediatrics
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 気管支喘息 / 免疫寛容 / 気道過敏性 / 気道炎症 / アレルギー |
|---|
| Research Abstract |
Oral administration of soluble antigen before immunization induces peripheral tolerance and is effective in suppressing animal models of autoimmune diseases. However, few studies have focused on effects on Th-2 type diseases. Mice were sensitized to ovalbumin(OVA) and subsequently challenged with OVA via the airways, eliciting airway hyperresponsiveness(AHR) and airway inflammation. The feeding effects of OVA at different phases of the immune response were evaluated. Mice exposed to both multiple high dose feeding and multiple low dose feeding before sensitization with OVA failed to develop AHR or airway inflammation. High dose feeding of OVA also abrogated AHR and partially suppressed airway inflammation when initiated after sensitization with OVA, but prior to challenge ; low dose feeding partially suppressed AHR but did not affect the development of airway inflammation. High dose but not low dose feeding was effective on AHR when initiated even after challenge with OVA. These data indicate that the dose and phase of the response may be critical in dictating the effect of inducing oral tolerance on allergen-induced AHR and airway inflammation
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