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 Soulika, Scott I. Simon, Roslyn Rivkah Isseroff

Research output: Contribution to journalArticle

49 Citations (Scopus)

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

Fingerprint

Wound Healing
Adrenergic Receptors
Epinephrine
Catecholamines
Neutrophils
Up-Regulation
Wounds and Injuries
Interleukin-6
Hormones
Skin
Macrophage Activation
Macrophages
Repair
Chemical activation
Tissue
Inflammation
Imaging techniques

ASJC Scopus subject areas

  • Dermatology
  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

Catecholamine stress alters neutrophil trafficking and impairs wound healing by β 2 -adrenergic receptor-mediated Upregulation of Il-6. / Kim, Min Ho; Gorouhi, Farzam; Ramirez, Sandra; Granick, Jennifer L.; Byrne, Barbara A; Soulika, Athena; Simon, Scott I.; Isseroff, Roslyn Rivkah.

In: Journal of Investigative Dermatology, Vol. 134, No. 3, 03.2014, p. 809-817.

Research output: Contribution to journalArticle

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AU - Byrne, Barbara A

AU - Soulika, Athena

AU - Simon, Scott I.

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AB - 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.

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