| Project/Area Number |
09670885
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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 |
Dermatology
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| Research Institution | NAGASAKI UNIVERSITY |
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Principal Investigator |
KATAYAMA Ichiro NAGASAKI UNIV.MEDICINE PROFESSOR, 医学部, 教授 (80191980)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Kazuhiro NAGASAKI UNIV.MEDICAL HOSPITAL LECTURE, 医学部附属病院, 講師 (80170968)
HAMASAKI Yoichiro NAGASAKI UNIV.MEDICAL HOSPITAL ASSISTANT, 医学部附属病院, 助手 (10180936)
山本 憲嗣 長崎大学, 医学部・附属病院, 助手 (90240093)
竹中 基 長崎大学, 医学部, 助手 (30281207)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | SKIN / INFLAMMATION / CONTACT DERMATITIS / EXPERIMENT MODEL / GLUCOCORTICOID / CYTOKINE / IL1 / IL10 / ステロイド |
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| Research Abstract |
(1) INDUCTION OF AUGMENTED CONTACT SENSITIVITY REACTION BY LONG TERM APPLICATION OF TOPICAL GLUCOCORTICOID
We further analyzed the regulatory mechanisms of augmentation of contact sensitivity reaction by long-term application of topical steroid (9 times application on alternate days). In this system, we found that number of gamma delta' positive cells significantly increased in the regional lymph node and these cells might contribute on augmented skin reaction. In addition, long term topical application of glucocorticoid augmented IgE mediated anaphylactic reaction of the skin which suggests that glucocorticoid enhance various types of cutaneous inflammation.
(2) CYTOKNE PROFILES IN THE SKIN AFTER LONG TERM APPLICATION OF TOPICAL GLUCOCORTICOID
We found that local injection of supernavant obtained from freeze and thawed-kerarinocytes down regulated augmented skin reaction of glucocorticoid treated mouse which suggests that glucocotticoid might down regulate the production of anti-inflammatory molecules by keratinocytes or up regulate the production of proinfiammatoty cytokines. To clarify these points, local injections if IL10 or IL1ra clearly do unregulated glucocorticoid induced-augmented skin reaction, PCR ana1ysis and immunohistochemical analysis revealed down regulation of IL10 and upreguadon of IL1 alpha in the lesional keratinocytes of glucocorticoid induced augmented skin reaction.
(3) REGULATORY MECHANISMS OF GLUCOCORTICOID INDUCED UPREGULATION OF PROLNFLAMMATORY CYTOKINES.
We found that hydrocortison clearly augmented hapten(DNBS and TNBS)-induced proinflammatory cvtokine (IL1 a and 1L6) productions and NF kappa B expression by cultured human keratinocytes while down regulated IL10 production. These results indicate that iLlO plays important role in cutaneous inflammation. Further study is needed to clarify the role of IL10 in NF K B activation.
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