Catecholamine stress alters neutrophil trafficking and impairs wound healing by β 2 -adrenergic receptor-mediated Upregulation of Il-6

Min Ho Kim, Farzam Gorouhi, Sandra Ramirez, Jennifer L. Granick, Barbara A. Byrne, Athena M. Soulika, Scott I. Simon, R. Rivkah Isseroff

Research output: Contribution to journalArticlepeer-review

55 Scopus citations

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 β 2 -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.

Original languageEnglish (US)
Pages (from-to)809-817
Number of pages9
JournalJournal of Investigative Dermatology
Volume134
Issue number3
DOIs
StatePublished - Mar 2014

Bibliographical note

Funding Information:
This work was supported by California Institute for Regenerative (CIRM) grant TG2-01163 (FG), NIH NIAID RO1 AI47294 (SIS), VA Merit Surg-016-06F, CIRM TR2-01787, and NIH R33 AI080604 (RRI).

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