Morphine induced exacerbation of sepsis is mediated by tempering endotoxin tolerance through modulation of miR-146a.
Morphine induced exacerbation of sepsis is mediated by tempering endotoxin tolerance through modulation of miR-146a.
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DOI：
10.1038/srep01977
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发表时间：
2013
影响因子：
4.6
通讯作者：
Roy, Sabita
中科院分区：
文献类型：
--
作者：
Banerjee, Santanu;Meng, Jingjing;Das, Subhas;Krishnan, Anitha;Haworth, Justin;Charboneau, Richard;Zeng, Yan;Ramakrishnan, Sundaram;Roy, Sabita
发展对内毒素的耐受性可防止全身感染期间持续的过度炎症。在这里，我们首次报道了慢性吗啡治疗降低内毒素耐受性，导致持续性炎症、败血症和败血症休克。吗啡可下调内毒素/脂多糖诱导的巨噬细胞miR-146a和155的表达。然而，只有miR-146a的过度表达，而不是miR-155的过度表达，才能消除吗啡介导的炎症反应。相反，拮抗miR-146a(但不是miR-155)会增加吗啡介导的超炎症反应的严重程度。这些结果表明miR-146a在临床和/或娱乐使用吗啡时作为一个分子开关控制超炎症反应。
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.
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影响因子：
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作者：
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通讯作者：
Golub, TR
影响因子：
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作者：
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