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Sci Rep. 2013;3:1977. doi: 10.1038/srep01977.

Morphine induced exacerbation of sepsis is mediated by tempering endotoxin tolerance through modulation of miR-146a.

Author information

1
Department of Surgery, University of Minnesota, Minneapolis, MN 55455, USA.

Abstract

Development of tolerance to endotoxin prevents sustained hyper inflammation during systemic infections. Here we report for the first time that chronic morphine treatment tempers endotoxin tolerance resulting in persistent inflammation, septicemia and septic shock. Morphine was found to down-regulate endotoxin/LPS induced miR-146a and 155 in macrophages. However, only miR-146a over expression, but not miR-155 abrogates morphine mediated hyper-inflammation. Conversely, antagonizing miR-146a (but not miR-155) heightened the severity of morphine-mediated hyper-inflammation. These results suggest that miR-146a acts as a molecular switch controlling hyper-inflammation in clinical and/or recreational use of morphine.

PMID:
23756365
PMCID:
PMC3679508
DOI:
10.1038/srep01977
[Indexed for MEDLINE]
Free PMC Article

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