Elucidation of pathophysiology of pruritic dermatosis and development of treating medicine

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461706
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• Research Institution: Yokohama City University
• Principal Investigator: AIHARA Michiko 横浜市立大学, 医学(系)研究科(研究院), 教授 (90231753)
• Co-Investigator(Kenkyū-buntansha): GOSHIMA Yoshio 横浜市立大学, 医学(系)研究科(研究院), 教授 (00153750) ; IZUHARA Kenji 佐賀大学, 医学部, 教授 (00270463)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: アトピー性皮膚炎 / かゆみ / コラーゲントリペプチド / セマフォリン3A

Outline of Final Research Achievements

Atopic dermatitis is a highly pruritic disease. We assessed effects of collagen tripeptide (CTP);a highly purified, non-antigenic, low allergenic collagen fraction. Because CTP had been shown to have some effects on nerve growth factor (NGF) and semaphorin-3A (Sema3A) to suppress C-fiber extension in mice skin. In the results, CTP suppressed production of TARC, MDS, TSLP in keratinocytes cultured with inflammatory and Th2 cytokines. In AD patients, CTP-administration for 3 months suppressed pruritus. In conclusion, CTP administration may useful for AD treatment, especially to control pruritus.
Periostin (PO) plays an important role in AD. We assessed effects of PO on the cultured cells. In the results, PO suppressed Sema3A production and promoted NGF production in the fibroblast and increased IL-18 and TNF-αproduction in peripheral mononuclear cells. PO may affect pruritus and immune cells in AD patients.

Free Research Field

皮膚科学、アレルギー学