A Mycobacterium tuberculosis mutant lacking the groEL homologue cpn60.1 is viable but fails to induce an inflammatory response in animal models of infection
A Mycobacterium tuberculosis mutant lacking the groEL homologue cpn60.1 is viable but fails to induce an inflammatory response in animal models of infection
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DOI：
10.1128/iai.01078-07
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发表时间：
2008-04-01
影响因子：
3.1
通讯作者：
Coates, Anthony R. M.
中科院分区：
文献类型：
--
作者：
Hu, Yanmin;Henderson, Brian;Coates, Anthony R. M.
结核病的病原体结核分枝杆菌具有两种伴侣蛋白（Cpn60）和一种辅伴侣蛋白（Cpn10）。我们在这里表明，cpn60.2和cpn10，但不是cpn60.1，是细胞生存所必需的。缺乏Cpn60.1的突变体在平板和肉汤培养中以及海洋巨噬细胞内与野生型生物体无法区分，尽管它对高温（55 ℃）的敏感性增加。然而，用Delta cpn60.1突变体感染小鼠揭示了与野生型生物体的主要差异。尽管在感染部位有相同数量的细菌，但Delta cpn60.1突变体在小鼠或豚鼠中均未能产生肉芽肿性炎症。这与感染动物和巨噬细胞中细胞因子表达减少有关。突变株细胞壁脂酸组成没有改变。因此，Cpn60.1似乎是调节M.肺结核感染。
The causative agent of tuberculosis, Mycobacterium tuberculosis, has two chaperonin (Cpn60) proteins and one cochaperonin (Cpn10) protein. We show here that cpn60.2 and cpn10, but not cpn60.1, are essential for cell survival. A mutant lacking Cpn60.1 was indistinguishable from the wild-type organism in plate and broth culture and within marine macrophages, although it showed increased sensitivity to high temperature (55 degrees C). However, infection of mice with the Delta cpn60.1 mutant revealed a major difference from the wild-type organism. In spite of having equal numbers of bacteria in infected sites, the Delta cpn60.1 mutant failed to produce granulomatous inflammation in either mice or guinea pigs. This was associated with reduced cytokine expression in infected animals and macrophages. Cell wall lipid acid composition was not altered in the mutant strain. Thus, it appears that Cpn60.1 is an important agent in the regulation of the cytokine-dependent granulomatous response in M. tuberculosis infection.