Interleukin-10 controls human peripheral PMN activation triggered by lipopolysaccharide
Interleukin-10 controls human peripheral PMN activation triggered by lipopolysaccharide
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DOI：
10.1016/j.cyto.2013.03.025
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发表时间：
2013-06-01
期刊：
影响因子：
3.8
通讯作者：
Fernandez, Gabriela C.
中科院分区：
文献类型：
--
作者：
Martire-Greco, Daiana;Rodriguez-Rodrigues, Nahuel;Fernandez, Gabriela C.
脓毒症早期会产生大量的抗炎介质，如白介素10。我们利用体外模型探讨了IL-10在中性粒细胞(PMN)激活/功能中的作用。分离的人PMN与脂多糖(LPS)和/或IL-10预先孵育18h，然后进行第二次LPS暴露，2 h后检测CD11b和CD66b的表达上调，并检测活性氧(ROS)的产生。我们发现，IL-10可抑制首次接触脂多糖所致的PMN活化及分泌肿瘤坏死因子-α和IL-8。在没有IL-10的情况下，第二次内毒素暴露引起的相加效应被IL-10阻止。只有ROS的产生受到PMN分泌的肿瘤坏死因子-α或IL-8的阻断的高度影响。此外，IL-10还阻止了内毒素启动的其他可能机制。因此，IL-10调节PMN的激活，阻止自分泌激活环和启动机制，使PMN对第二次脂多糖暴露的反应较弱。(C)2013爱思唯尔有限公司。保留所有权利。
Large amounts of anti-inflammatory mediators, such as interleukin (IL)-10, are produced and found early in the course of sepsis. We explore the role of IL-10 on neutrophil (PMN) activation/function using an in vitro model. Isolated human PMN were pre-incubated with lipopolysaccharide (LPS) and/or IL-10 for 18 h. Subsequently, a second LPS exposure was performed and CD11b and CD66b up-regulation, and the reactive oxygen species (ROS) generation were measured 2 h later. We found that IL-10 prevented PMN activation and the secretion of TNF-alpha and IL-8 induced by the first LPS contact. In the absence of IL-10, a second LPS exposure induced additive effects that were prevented by IL-10. Only ROS generation was highly affected by the blockade of PMN-secreted TNF-alpha or IL-8. Additionally, IL-10 prevented other possible mechanisms of LPS priming. Therefore, IL-10 modulates PMN activation preventing autocrine activating loops and priming mechanisms, rendering PMN less responsive to a second LPS exposure. (C) 2013 Elsevier Ltd. All rights reserved.