2011 Fiscal Year Final Research Report
Establishment of new molecular therapy of keloid and elucidation of mechanism of development by IL-23/IL-17 pathway
| Project/Area Number |
21592298
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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 |
Plastic surgery
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| Research Institution | Nippon Medical School |
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Principal Investigator |
TOSA Mamiko 日本医科大学, 医学部, 助教 (30301568)
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| Co-Investigator(Kenkyū-buntansha) |
MOHAMMAD Ghazizadeh 日本医科大学, 老人病研究所, 准教授 (30190979)
MURAKAMI Masahiro 日本医科大学, 医学部, 准教授 (00239500)
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| Project Period (FY) |
2009 – 2011
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| Keywords | ケロイド / IL-17 / IL-23 / ケロイドモデル |
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| Research Abstract |
We have reported that IL-6 mediated inflammation is a key player and may be considered as a common causative factor for development of keloid. IL-17, a recently discovered pro-inflammatory cytokine, is secreted by a distinct subtype of activated CD4 T-cells known as Th17.We first examined the distribution of Th17 cells in peripheral blood and keloid tissues obtained from the patients. There was an increased in Th17 cells as compared with normal individuals. The expression of IL-17 gene in keloid derived fibroblasts(KF) was higher than in normal dermis derived fibroblasts(NF). We measured mRNA expressions of two principal ECM molecules, COL1A2 and FN1, in NF cultures after addition of IL-17A peptide or in KF cultures after inhibition of IL-17 with anti-IL-17 antibody at various concentrations. Addition of IL-17A in NF culture medium significantly and dose-dependently enhanced COL1A2 and FN1 mRNA expressions, whereas inhibition of IL-17 by anti-IL-17 antibody in KF culture medium lowered COL1A2 and FN1 mRNA expressions. Our results indicate that IL-17 signaling may play an integral role in keloid pathogenesis and provide clues for development of IL-17 blocking strategies for therapy or prophylaxis of keloid.
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