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J Surg Res. 2009 Apr;152(2):311-8. doi: 10.1016/j.jss.2008.05.001. Epub 2008 Jun 2.

Norepinephrine-mediated suppression of phagocytosis by wound neutrophils.

Author information

  • 1Burn and Shock Trauma Institute, Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, Maywood, Illinois, USA.

Abstract

BACKGROUND:

The systemic response to injury is characterized by massive release of norepinephrine (NE) into the circulation as a result of global sympathetic activation. Multiple authors have demonstrated NE-mediated alterations in migration of circulating neutrophils to wounds. We hypothesized that NE further alters wound neutrophil phagocytic function through adrenergic signaling pathways.

METHODS:

A standard subcutaneous sponge wound model was used. Murine wound neutrophils were harvested at 24 and 120 h after injury and treated with physiological (10(-9) M) and pharmacologic (10(-6) M) doses of NE. Phagocytosis of green fluorescent protein-labeled Escherichia coli was assayed by flow cytometry. The signaling pathways mediating NE modulation of phagocytosis by wound neutrophils were defined by pharmacologic manipulation of alpha- and beta-adrenoreceptors and protein kinase A.

RESULTS:

Pharmacologic-dose NE, but not-physiological-dose NE, suppressed the phagocytic efficiency of 120-h wound neutrophils. This alteration in phagocytic efficiency appears to be mediated through alpha- and beta- adrenoreceptors and downstream protein kinase A. Phagocytosis by 24-h wound neutrophils was not impacted by NE treatment.

CONCLUSIONS:

The present study is the first to demonstrate NE-mediated alterations in the process of phagocytosis by wound neutrophils. We conclude that NE plays a temporally and dose-defined immunomodulatory role in cutaneous wound healing through alterations in phagocytosis by wound neutrophils and may represent a target for therapeutic manipulation of the innate immune response.

PMID:
18952237
[PubMed - indexed for MEDLINE]
PMCID:
PMC2683017
Free PMC Article

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