| Project/Area Number |
16590099
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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 |
Environmental pharmacy
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| Research Institution | Kobe Pharmaceutical University |
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Principal Investigator |
YOSHINO Shin Kobe Pharmaceutical University, Pharmacy, professor, 薬学部, 教授 (00260729)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Kosa / Th1 / Th2 / oral tolerance / cytokine / allergy / 免疫寛容 / 食物アレルギー / 自己免疫疾患 |
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| Research Abstract |
The effects of Kosa on Th1 and Th2 immune responses and on oral tolerance in mice were investigated. Th1 responses appear to be involved in some of autoimmune diseases such as rheumatoid arthritis and Th2 in allergic diseases including pollen-induced rhinitis. Oral tolerance appears to play an important role in preventing food allergy. To induce Th1 and Th2 immune responses, DBA mice were immunized with ovalbumin (OVA) (day 0). On day 21, anti-OVA IgG2a antibodies and IFN-g were measured as indicators of Th1 immune responses and anti-OVA IgG1 and IgE antibodies and IL-4 as those of Th2 immune responses. TGF-b and IL-10 were also measured as indicators Th3-and regulatory T cell-mediated immune responses, respectively. Th1 and Th2 oral tolerance were induced by feeding mice 20 and 0.1 mg of OVA, respectively, from days-5 to-1. Varying doses of Kosa were orally administered daily over a period of 21 days commencing on day 0 to test its effects on Th1 and Th2 responses. To examine the effect of Kosa on oral tolerance, Kosa were orally given daily from days-5 to -1. PBS was fed as a control. The results showed that Kosa failed to affect production of anti-OVA IgG2a and IFN-g. In contrast, anti-OVA IgE and IL-4 secretion was facilitated by Kosa, although anti-OVA IgGl production was unaffected by Kosa. There was no difference in production of TGF-b and IL-10 between Kosa and PBS-treated mice. Th2 but not Th1 oral tolerance appeared to be enhanced by Kosa. These results suggest that Kosa may facilitate Th2 but not Th1 immune responses. Th2 but not Th1 oral tolerance also may be enhanced by Kosa. The function of Th3 and regulatory T cells does not appear to be affected by Kosa.
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