Living on the edge: inhibition of host cell apoptosis by Mycobacterium tuberculosis.

Living on the edge: inhibition of host cell apoptosis by Mycobacterium tuberculosis.
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DOI:
10.2217/17460913.3.4.415
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发表时间:
2008-08
影响因子:
3.1
通讯作者:
Miller JL
Miller JL
中科院分区:
生物学3区
文献类型:
--
作者:
Briken V;Miller JL

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结核病是由结核分枝杆菌感染引起的一种具有全球重要性的人类疾病。因此,估计有三分之一的世界人口处于潜伏感染状态;每年有200万至300万人死亡,耐多药和极端耐药结核病病例数量不断增加。结核分枝杆菌是一种高度适应的人类病原体,它已经进化到采用多种策略来试图避免有效的宿主免疫反应。诱导宿主细胞死亡是一种古老的免疫防御策略,在整个动物和植物王国中都是保守的。本文就分枝杆菌与宿主细胞相互作用诱导宿主细胞凋亡的研究现状进行综述。我们得出结论,结核分枝杆菌的毒力菌株采用几种策略来避免诱导巨噬细胞死亡,这一过程的成功显然对细菌毒力很重要。宿主细胞凋亡抑制的分子机制尚不清楚,但最近在结核分枝杆菌基因组中发现的抗凋亡基因为研究这种宿主-病原体相互作用的细节提供了必要的工具。这些未来研究的结果可能对开发新的药物靶点和/或候选疫苗有用。
Tuberculosis is a human disease of global importance caused by infection with Mycobacterium tuberculosis. Thus, an estimated one-third of the world's population is latently infected; there are 2-3 million annual deaths and an increasing amount of multi-drug resistant and extreme-drug resistant tuberculosis cases. M. tuberculosis is a highly adapted human pathogen that has evolved to employ multiple strategies in its attempt to avoid an efficient host immune response. The induction of host cell death is an ancient immune defense strategy that is conserved throughout the animal and plant kingdoms. Here we review the current status of the research involving interaction of mycobacteria with host cells regarding the induction of host cell death by apoptosis. We conclude that virulent strains of M. tuberculosis employ several strategies to avoid the induction of macrophage cell death and success in this process is clearly important for bacterial virulence. The molecular mechanisms of host cell apoptosis inhibition are little understood, but the recent identification of anti-apoptosis genes in the genome of M. tuberculosis has provided the tools necessary to investigate the details of this host-pathogen interaction. The results of these future studies may prove useful for the development of new drug targets and/or vaccine candidates.
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影响因子: 15.9
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发表时间: 2007-08-01
期刊: MYCOPATHOLOGIA
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