...
首页> 外文期刊>Infection and immunity >Streptococcus pneumoniae-Induced Caspase 6-Dependent Apoptosis in Lung Epithelium
【24h】

Streptococcus pneumoniae-Induced Caspase 6-Dependent Apoptosis in Lung Epithelium

机译:肺炎链球菌诱导的肺上皮细胞中胱天蛋白酶6依赖性凋亡

获取原文
           

摘要

Streptococcus pneumoniae is the major pathogen of community-acquired pneumonia and one of the most common causes of death due to infectious diseases in industrialized countries. Lung epithelium lines the airways and constitutes the first line of innate defense against respiratory pathogens. Little is known about the molecular interaction of pneumococci with lung epithelial cells. Apoptosis of lung epithelium is involved in some bacterial lung infections. In this study different pneumococcal strains specifically induced either apoptotic or necrotic death of human alveolar and bronchial epithelial cells. Pneumococcus-induced apoptosis did not depend on the virulence factors pneumolysin and H2O2. Apoptotic cells showed increased activity of caspases 6, 8, and 9 but not increased activity of caspase 3. Moreover, programmed cell death could be strongly reduced by a caspase 6 inhibitor and a pan-caspase inhibitor. Inhibitors of calpain and chymotrypsin- and trypsin-like proteases also reduced pneumococcus-induced apoptosis. Furthermore, pneumococcus-infected human alveolar epithelial cells showed Bid cleavage and reduced levels of Bcl2 and Bax. Overexpression of Bcl2 in these cells reduced apoptosis significantly. Thus, pneumococci induced apoptosis of human alveolar and bronchial epithelial cells. Programmed cell death was executed by caspase 6 and noncaspase proteases, but not by caspase 3, and could be blocked by overexpression of Bcl2.
机译:肺炎链球菌是社区获得性肺炎的主要病原体,也是工业化国家因传染病导致的最常见死亡原因之一。肺上皮细胞覆盖呼吸道,构成抵抗呼吸道病原体的先天防御。关于肺炎球菌与肺上皮细胞的分子相互作用知之甚少。肺上皮细胞的凋亡与某些细菌性肺部感染有关。在这项研究中,不同的肺炎球菌菌株特异性诱导人肺泡和支气管上皮细胞凋亡或坏死。肺炎球菌诱导的细胞凋亡不依赖于肺炎球菌溶血素和H 2 O 2 的致病因子。凋亡细胞显示胱天蛋白酶6、8和9的活性增加,但胱天蛋白酶3的活性未增加。此外,胱天蛋白酶6抑制剂和泛胱天蛋白酶抑制剂可大大降低程序性细胞死亡。钙蛋白酶和胰凝乳蛋白酶以及胰蛋白酶样蛋白酶的抑制剂也减少了肺炎球菌诱导的细胞凋亡。此外,肺炎球菌感染的人肺泡上皮细胞显示出Bid裂解和Bcl2和Bax水平降低。这些细胞中Bcl2的过表达显着降低了细胞凋亡。因此,肺炎球菌诱导人肺泡和支气管上皮细胞凋亡。程序性细胞死亡是由caspase 6和noncaspase蛋白酶执行的,而不是由caspase 3执行的,并且可能被Bcl2的过表达所阻止。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号