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

Authors
  • Kim, Min-Ho1
  • Gorouhi, Farzam2
  • Ramirez, Sandra2
  • Granick, Jennifer L3
  • Byrne, Barbara A3
  • Soulika, Athena M4
  • Simon, Scott I5
  • Isseroff, Rivkah R6
  • 1 Department of Biomedical Engineering, University of California at Davis, Davis, California, USA; Department of Biological Sciences, Kent State University, Kent, Ohio, USA.
  • 2 Department of Dermatology, School of Medicine, University of California at Davis, Davis, California, USA.
  • 3 School of Veterinary Medicine: Pathology, Microbiology, Immunology, University of California at Davis School of Veterinary Medicine, Davis, California, USA.
  • 4 Department of Dermatology, School of Medicine, University of California at Davis, Davis, California, USA; Shriners Hospital of Northern California, Sacramento, California, USA.
  • 5 Department of Biomedical Engineering, University of California at Davis, Davis, California, USA.
  • 6 Department of Dermatology, School of Medicine, University of California at Davis, Davis, California, USA; Dermatology Section, Department of Veterans Affairs, Northern California Health Care System, Mather, California, USA. Electronic address: [email protected].edu.
Type
Published Article
Journal
Journal of Investigative Dermatology
Publisher
Elsevier
Publication Date
Mar 01, 2014
Volume
134
Issue
3
Pages
809–817
Identifiers
DOI: 10.1038/jid.2013.415
PMID: 24121404
Source
Medline
Language
English
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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