| First Author | Kim MH | Year | 2014 |
| Journal | J Invest Dermatol | Volume | 134 |
| Issue | 3 | Pages | 809-817 |
| PubMed ID | 24121404 | Mgi Jnum | J:206071 |
| Mgi Id | MGI:5547859 | Doi | 10.1038/jid.2013.415 |
| Citation | Kim MH, et al. (2014) Catecholamine Stress Alters Neutrophil Trafficking and Impairs Wound Healing by beta2-Adrenergic Receptor-Mediated Upregulation of IL-6. J Invest Dermatol 134(3):809-17 |
| abstractText | 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 beta2-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. |
