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. In conclusion, catecholamines released by the sympathetic nervous system stimulate mast cells to secrete anti-inflammatory cytokines that impair inflammatory cell mobilization, leading to a delay in the resolution of wound healing under stress conditions. [Display omitted] •Chronic stress increases mast cells mobilization during skin wound healing in mice.•Chronic stress enhances sympathetic innervation in skin wound healing in vivo.•Chronic stress promotes an anti-inflammatory response in skin wound healing in vivo.•Mast cells increase IL-10 release and degranulation under stress conditions in vitro.•Neuroimmune crosstalk contributes to delayed skin wound healing induced by stress.