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首页> 外文期刊>Cellular Physiology and Biochemistry >IL-33 Attenuates Sepsis by Inhibiting IL-17 Receptor Signaling through Upregulation of SOCS3
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IL-33 Attenuates Sepsis by Inhibiting IL-17 Receptor Signaling through Upregulation of SOCS3

机译：IL-33通过上调SOCS3抑制IL-17受体信号传导来减轻脓毒症

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>Background/Aims: Sepsis is a systemic inflammatory response during infection. There are limited therapeutic options for sepsis patients. Interleukin (IL)-33 has been reported recently with a beneficial effect in mouse sepsis. Methods: In this study, we initiated a clinical study to measure serum levels of pro-inflammatory cytokines including IL-33 in sepsis patients. Next, we employed cecal ligation and puncture (CLP) to study the role of IL-33 during sepsis. To further dissect the molecular mechanism, we used in vivo knockout models and in vitro knockdown murine embryonic fibroblasts (MEFs) to investigate the cross-talk between IL-33 and IL-17 signaling, and to identify the potential downstream mediators. Results: IL-33 and IL-17 were upregulated in both clinical and experimental sepsis. In CLP, IL-33 (-/-) mice showed higher mortality rate, and IL-33 treatment improved the survival rate. Elevated proinflammatory cytokines in sepsis were related to IL-17 from ?3?′T cells. IL-33 treatment suppressed production of these cytokines by targeting IL-17 signaling both in vivo and in vitro. Finally, IL-33 was shown to inhibit the IL-17 pathway via activating suppressor of cytokine signaling (SOCS)-3. Conclusion: Collectively, the results suggest that IL-33 plays a negative regulatory role in sepsis progression by inhibiting IL-17 pathway through activating SOCS3. This finding would inspire a new therapeutic strategy for treating sepsis.
机译：> 背景/目的： 败血症是感染过程中的全身性炎症反应。败血症患者的治疗选择有限。最近报道了白介素（IL）-33在小鼠败血症中具有有益作用。 方法： 在这项研究中，我们启动了一项临床研究，以测量败血症患者的促炎性细胞因子（包括IL-33）的血清水平。接下来，我们采用盲肠结扎穿刺术（CLP）来研究IL-33在脓毒症中的作用。为了进一步剖析分子机制，我们使用了体内敲除模型和体外敲除小鼠胚胎成纤维细胞（MEFs）来研究IL-33和IL-33之间的串扰。 17信令，并识别潜在的下游介体。 结果： 在临床和实验性脓毒症中，IL-33和IL-17均被上调。在CLP中，IL-33（-/-）小鼠显示出较高的死亡率，而IL-33治疗可提高存活率。脓毒症中促炎细胞因子的升高与来自？3？'T细胞的IL-17有关。 IL-33治疗通过靶向IL-17体内和体外的信号传导抑制了这些细胞因子的产生。最后，IL-33被证明可通过激活细胞因子信号传导抑制因子（SOCS）-3抑制IL-17途径。 结论： 总的来说，该结果表明IL-33通过激活SOCS3抑制IL-17途径，在败血症进展中起负调控作用。这一发现将为治疗败血症提供新的治疗策略。

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