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首页> 外文期刊>Infection and immunity >Mycobacterium tuberculosis Triggers Apoptosis in Peripheral Neutrophils Involving Toll-Like Receptor 2 and p38 Mitogen Protein Kinase in Tuberculosis Patients
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Mycobacterium tuberculosis Triggers Apoptosis in Peripheral Neutrophils Involving Toll-Like Receptor 2 and p38 Mitogen Protein Kinase in Tuberculosis Patients

机译：结核分枝杆菌触发外周血中性粒细胞的凋亡，涉及结核病患者中的Toll样受体2和p38丝裂原蛋白激酶。

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Polymorphonuclear neutrophils (PMN) exposed to Mycobacterium tuberculosis display bactericidal responses and produce inflammatory proteins. This PMN-mediated inflammatory response is regulated by an activation of the apoptotic program, which collaborates to avoid tissue injury. In vitro, circulating PMN from patients with tuberculosis (TB) show an increased spontaneous apoptosis, and M. tuberculosis-induced activation accelerates the PMN apoptosis. In this study, we evaluated the mechanisms involved in spontaneous and M. tuberculosis-induced apoptosis. We demonstrate that apoptosis of PMN is not induced by lipoarabinomannan or by a whole-cell lysate of M. tuberculosis and that neither tumor necrosis factor alpha nor CD11b, CD14, and Fcγ receptors are involved. Apoptosis of PMN from patients with active TB (TB-PMN) is induced by the interaction with the whole M. tuberculosis via Toll-like receptor 2 (TLR2), and, in contrast to spontaneous apoptosis, it involves the p38 mitogen-activated protein kinase (MAPK) pathway. These results correlate with a high expression of phosphorylated p38 (p-p38) in circulating TB-PMN and with the ability of M. tuberculosis to induce in vitro the expression of p-p38 in PMN. Therefore, when the bacterial burden is low, TB-PMN could be detecting nonopsonized M. tuberculosis via TLR2, leading to the activation of the p38 MAPK pathway, which in turn would induce PMN activation and apoptosis. This mechanism needs further confirmation at the site of infection.
机译：暴露于结核分枝杆菌的多形核中性粒细胞（PMN）表现出杀菌反应并产生炎症蛋白。 PMN介导的炎症反应是通过凋亡程序的激活来调节的，凋亡程序的协作可避免组织损伤。在体外，来自肺结核（TB）患者的循环PMN显示自发凋亡增加， M。结核诱导的激活促进了PMN的凋亡。在这项研究中，我们评估了自发性和 M的机制。结核诱导的细胞凋亡我们证明，脂蛋白甘露聚糖或 M的全细胞裂解液不会诱导PMN的凋亡。并没有涉及肿瘤坏死因子α和CD11b，CD14和Fcγ受体。与整个 M的相互作用诱导了活动性结核病患者的PMN凋亡（TB-PMN）。通过Toll样受体2（TLR2）感染结核病，并且与自发凋亡相反，它涉及p38丝裂原活化蛋白激酶（MAPK）途径。这些结果与循环TB-PMN中磷酸化p38（p-p38）的高表达以及 M的能力有关。结核在体外诱导PMN中p-p38的表达。因此，当细菌负担很低时，TB-PMN可以检测到非调理的 M。 TLR2介导结核病，导致p38 MAPK通路活化，进而诱导PMN活化和细胞凋亡。该机制需要在感染部位进一步确认。

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