抑制Toll样受体9通过抑制过度的炎症反应减轻脓毒症诱导的死亡率。
Inhibition of Toll-like receptor 9 attenuates sepsis-induced mortality through suppressing excessive inflammatory response.
作者信息
Hu Dan, Yang Xiaohua, Xiang Yanxiao, Li Hui, Yan Hui, Zhou Jun, Caudle Yi, Zhang Xiumei, Yin Deling
机构信息
Department of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, TN, USA; Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, China.
Department of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, TN, USA.
出版信息
Cell Immunol. 2015 Jun;295(2):92-8. doi: 10.1016/j.cellimm.2015.03.009. Epub 2015 Mar 31.
Sepsis, a major clinical problem with high morbidity and mortality, is caused by overwhelming systemic host-inflammatory response. Toll-like receptors (TLRs) play a fundamental role in induction of hyperinflammation and tissue damage in sepsis. In this study, we demonstrate a protective role of TLR9 inhibition against the dysregulated inflammatory response and tissue injury in sepsis. TLR9 deficiency decreased the mortality of mice following cecal ligation and puncture (CLP)-induced sepsis. TLR9 knockout mice showed dampened p38 activation and augmented Akt phosphorylation in the spleen, lung and liver. In addition, TLR9 deficiency decreased the levels of inflammatory cytokines and attenuated splenic apoptosis after CLP. These results indicate that TLR9 inhibition might offer a novel therapeutic strategy for the management of sepsis.
脓毒症是一个具有高发病率和死亡率的主要临床问题，由全身性宿主炎症反应失控引起。Toll样受体（TLR）在脓毒症中过度炎症反应和组织损伤的诱导中起基本作用。在本研究中，我们证明了抑制TLR9对脓毒症中失调的炎症反应和组织损伤具有保护作用。TLR9缺陷降低了盲肠结扎和穿刺（CLP）诱导的脓毒症小鼠的死亡率。TLR9基因敲除小鼠在脾脏、肺和肝脏中显示出p38激活减弱和Akt磷酸化增强。此外，TLR9缺陷降低了CLP后炎症细胞因子水平并减轻了脾脏细胞凋亡。这些结果表明，抑制TLR9可能为脓毒症的治疗提供一种新的策略。
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