Repeated stress-induced crosstalk between the sympathetic nervous system and mast cells contributes to delayed cutaneous wound healing in mice

The study identifies a link between the neuroimmune interaction and the impairment of wound healing induced by repeated stress. Stress increased mast cell mobilization and degranulation, levels of IL-10, and sympathetic reinnervation in mouse wounds. In contrast to mast cells, macrophage infiltration into wounds was significantly delayed in stressed mice. Chemical sympathectomy and the blockade of mast cell degranulation reversed the effect of stress on skin wound healing in vivo. In vitro, high epinephrine levels stimulated mast cell degranulation and IL-10 release.
Source: Journal of Neuroimmunology - Category: Allergy & Immunology Authors: Source Type: research