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

Bruna Romana-Souza; Lin Chen; Luisa A DiPietro

doi:10.1016/j.jneuroim.2023.578104

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

J Neuroimmunol. 2023 Jun 15:379:578104. doi: 10.1016/j.jneuroim.2023.578104. Epub 2023 May 11.

Authors

Bruna Romana-Souza¹, Lin Chen², Luisa A DiPietro²

Affiliations

¹ Department of Histology and Embryology, Rio de Janeiro State University, Rio de Janeiro, Brazil. Electronic address: bruna.romana.souza@uerj.br.
² Center for Wound Healing and Tissue Regeneration, University of Illinois Chicago, Chicago, IL, USA.

PMID: 37196594
DOI: 10.1016/j.jneuroim.2023.578104

Abstract

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.

Keywords: Catecholamine; Mast cells; Neurogenic inflammation; Stress; Wound healing.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Interleukin-10* / metabolism
Mast Cells* / metabolism
Mice
Skin / injuries
Skin / metabolism
Sympathetic Nervous System
Wound Healing / physiology

Substances

Interleukin-10