The crosstalk between peripheral nerves and immune cells in the pathogenesis of pruritic skin diseases.

2015 Fiscal Year Final Research Report

• Project/Area Number: 26893128
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Dermatology
• Research Institution: Kyoto University
• Principal Investigator: Nakashima Chisa 京都大学, 医学(系)研究科(研究院), 助教 (50733573)
• Project Period (FY): 2014-08-29 – 2016-03-31
• Keywords: 皮膚 / 掻痒

Outline of Final Research Achievements

Epidermal hyperinnervation is one commonly discussed factor underlying pruritus in the patients with atopic dermatitis (AD). Overexpression of axonal guidance molecules in the epidermis has been reported to regulate epidermal hyperinnervation, which elongates the nerve fibers into the epidermis and is considered to drive the pruritic sensation. Vascular endothelial growth factor (VEGF), which regulates blood and lymphatic vessels development, is known to be involved in the pathogenesis of psoriasis. Moreover, VEGF-A has a neurotrophic effect, which causes profuse neutrite outgrowth of the dorsal root ganglion. To address the mechanism of pruritus in psoriasis, we used an imiquimod (IMQ)-induced psoriasiform dermatitis mouse model. Our study suggests that the upregulation of VEGF-A in the IMQ-induced psoriasiform dermatitis mouse model promotes epidermal hyperinnervation. These findings suggest that VEGF-A may be involved in the pathophysiology of pruritus in psoriasis.

Free Research Field

皮膚科