Enhanced nerve-mast cell interaction mediated by cell adhesion molecule 1 in stress-related diseases

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590492
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Kinki University
• Principal Investigator: ITO Akihiko 近畿大学, 医学部, 教授 (80273647)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 接着分子 / 神経‐免疫相互作用 / アトピー性皮膚炎 / 脱顆粒 / 細胞間接着力

Outline of Final Research Achievements

Neuroimmunological disorders are involved in the pathogenesis of atopic dermatitis (AD), partly through enhanced sensory nerve-skin mast cell interaction. Cell adhesion molecule 1 (CADM1) is known to mediate nerve-mast cell interaction. In a hapten-induce AD mouse model, AD-like lesional mast cells expressed three-fold more CADM1 transcripts than non-lesional mast cells. In nerve-mast cell coculture, CADM1 overexpression in IC2 mast cells strengthened dorsal root ganglion neurite-IC2 cell adhesion and doubled the population of IC2 cells responding to nerve activation. Increased expression of CADM1 in mast cells appeared to be a cause of enhanced sensory nerve-mast cell interaction in a hapten-induced AD mouse model, and might be involved in stress-induced deterioration of human AD.

Free Research Field

実験病理学