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首页> 外文期刊>Cellular immunology >Activation of apoptosis, but not necrosis, during Mycobacterium tuberculosis infection correlated with decreased bacterial growth: Role of TNF-alpha, IL-10, caspases and phospholipase A2
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Activation of apoptosis, but not necrosis, during Mycobacterium tuberculosis infection correlated with decreased bacterial growth: Role of TNF-alpha, IL-10, caspases and phospholipase A2

机译：结核分枝杆菌感染过程中细胞凋亡的激活而不是坏死与细菌生长减少有关：TNF-α，IL-10，胱天蛋白酶和磷脂酶A2的作用

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Monocyte/macrophage cell death is an important event during mycobacterial infection. To get insights about the influence of mononuclear phagocyte maturation in this event we compared the response to Mycobacterium tuberculosis (Mtb) infection of fresh isolated monocytes and monocyte-derived macrophages (MDM) from healthy tuberculin positive individuals. Both monocytes and MDM underwent apoptosis, however, there was a higher numbers of apoptotic macrophages with active Caspases 8 and 9. We also compared Mtb-induced cell death in U937 pro-monocytes and PMA-differentiated cells (U937D). In response to Mtb infection, U937D cells underwent apoptosis and promonocytes both apoptosis and necrosis. There were high number of U937D cells producing TNF-alpha and high number of IL-10(+) promonocytes. These evidences suggest that U937 could be a valid model to study the mechanisms that rule Mtb-induced cell death. Experiments with the cell line and fresh isolated mononuclear cells with pharmacological inhibitors showed that induction of necrosis involved calcium and cAMP signals resulting in IL-10 production. Necrosis also correlated with Caspase 3, PLA2 activity and bacterial growth. In U937D cells and monocytes from healthy donors there was activation of calcium, TNF-alpha and Caspase 8 activation and decreased bacterial load. Understanding the mechanisms that control the dichotomy events between apoptosis and necrosis/ oncosis associated with cell maturity might open new strategies to better control the course of mycobacterial infections. (C) 2007 Elsevier Inc. All rights reserved.
机译：单核细胞/巨噬细胞死亡是分枝杆菌感染期间的重要事件。为了获得关于单核吞噬细胞成熟在此事件中的影响的见解，我们比较了来自健康结核菌素阳性个体的新鲜分离的单核细胞和单核细胞衍生的巨噬细胞（MDM）对结核分枝杆菌（Mtb）感染的反应。单核细胞和MDM均发生凋亡，但是，凋亡的巨噬细胞中具有活跃的Caspases 8和9。我们还比较了U937前单核细胞和PMA分化细胞（U937D）中Mtb诱导的细胞死亡。响应Mtb感染，U937D细胞发生凋亡，而原核细胞发生凋亡和坏死。有大量产生TNF-α的U937D细胞和大量的IL-10（+）原代细胞。这些证据表明，U937可能是研究统治Mtb诱导的细胞死亡的机制的有效模型。细胞系和新鲜分离的单核细胞与药理抑制剂的实验表明，坏死的诱导涉及钙和cAMP信号，导致产生IL-10。坏死也与胱天蛋白酶3，PLA2活性和细菌生长有关。在来自健康供体的U937D细胞和单核细胞中，钙，TNF-α和Caspase 8的活化被激活，细菌载量降低。了解控制细胞凋亡与细胞成熟相关的坏死/肿瘤之间二分法事件的机制可能会为更好地控制分枝杆菌感染的进程打开新的策略。 （C）2007 Elsevier Inc.保留所有权利。

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