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.
| Original language | English |
|---|---|
| Article number | 1977 |
| Journal | Scientific Reports |
| Volume | 3 |
| DOIs | |
| State | Published - 8 Jul 2013 |
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Morphine induced exacerbation of sepsis is mediated by tempering endotoxin tolerance through modulation of miR-146a. / Banerjee, Santanu; Meng, Jingjing; Das, Subhas; Krishnan, Anitha; Haworth, Justin; Charboneau, Richard; Zeng, Yan; Ramakrishnan, Sundaram; Roy, Sabita.
In: Scientific Reports, Vol. 3, 1977, 08.07.2013.Research output: Contribution to journal › Article
TY - JOUR
T1 - Morphine induced exacerbation of sepsis is mediated by tempering endotoxin tolerance through modulation of miR-146a
AU - Banerjee, Santanu
AU - Meng, Jingjing
AU - Das, Subhas
AU - Krishnan, Anitha
AU - Haworth, Justin
AU - Charboneau, Richard
AU - Zeng, Yan
AU - Ramakrishnan, Sundaram
AU - Roy, Sabita
PY - 2013/7/8
Y1 - 2013/7/8
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84879623341&partnerID=8YFLogxK
U2 - 10.1038/srep01977
DO - 10.1038/srep01977
M3 - Article
C2 - 23756365
AN - SCOPUS:84879623341
VL - 3
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
M1 - 1977
ER -