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Catecholamine stress alters neutrophil trafficking and impairs wound healing by β2-adrenergic receptor-mediated upregulation of IL-6.

Authors
  • Mh, Kim
  • F, Gorouhi
  • S, Ramirez
  • Jl, Granick
  • Ba, Byrne
  • Athena Soulika
  • Si, Simon
  • Rr, Isseroff
Type
Published Article
Journal
Journal of Investigative Dermatology
Publisher
Elsevier
Volume
134
Issue
3
Pages
809–809
Identifiers
DOI: 10.1038/jid.2013.415
Source
Soulika Lab - UC Davis dermatology-ucdavis
License
Unknown

Abstract

Stress-induced hormones can alter the inflammatory response to tissue injury; however, the precise mechanism by which epinephrine influences inflammatory response and wound healing is not well defined. Here we demonstrate that epinephrine alters the neutrophil (polymorphonuclear leukocyte (PMN))-dependent inflammatory response to a cutaneous wound. Using noninvasive real-time imaging of genetically tagged PMNs in a murine skin wound, chronic, epinephrine-mediated stress was modeled by sustained delivery of epinephrine. Prolonged systemic exposure of epinephrine resulted in persistent PMN trafficking to the wound site via an IL-6-mediated mechanism, and this in turn impaired wound repair. Further, we demonstrate that β2-adrenergic receptor-dependent activation of proinflammatory macrophages is critical for epinephrine-mediated IL-6 production. This study expands our current understanding of stress hormone-mediated impairment of wound healing and provides an important mechanistic link to explain how epinephrine stress exacerbates inflammation via increased number and lifetime of PMNs.

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