| Project/Area Number |
04670453
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
OKAYAMA Hiroshi Tohoku Univ. First Department of Internal Medicine, School of Medicine, Assistant Proffessor, 医学部, 助手 (10160730)
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| Co-Investigator(Kenkyū-buntansha) |
TAMURA Gen Tohoku Univ. First Department of Internal Medicine, School of Medicine, Assistan, 医学部, 助手 (70188431)
SHIMURA Sanae Tohoku Univ. First Department of Internal Medicine, School of Medicine, Assistan, 医学部・付属病院, 講師 (20154312)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1992: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | IL-5 / IL-10 / glucocorticoid / human / monomuclear cell / gene expression / atopy / asthma / ステロイド / 喘息 |
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| Research Abstract |
The effect of glucocorticoids on interleukin 5 induction and its mechanism from normal and atopic human mononuclear cells
The effect of glucocorticoid, dexamethasone on IL-10 gene expression by human nonocytes, lymmphocytes and peripheral blood mononuclear cells (PBMC) from five healthy volunteers was examined. PBMC expressed IL-10 gene without stimulation and increased by PHA or LPS stimulation, which was suppressed by dexamethasone to 50%. The results indicate that IL-2, IL-4 and IL-5.
The results suggest that the regulation of IL-10 gene expression by dexamethasone is different from that of many cytokines. IL-10 may play an important role in the cytokine regulation of alloegie inflammation during glucocorticoid therapy.
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