Modulation of cell death by M. tuberculosis as a strategy for pathogen survival.
Modulation of cell death by M. tuberculosis as a strategy for pathogen survival.
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DOI：
10.1155/2011/678570
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发表时间：
2011
影响因子：
--
通讯作者：
Doherty TM
中科院分区：
文献类型：
--
作者：
Abebe M;Kim L;Rook G;Aseffa A;Wassie L;Zewdie M;Zumla A;Engers H;Andersen P;Doherty TM
已经清楚地证明，在体外，强毒的结核分枝杆菌可以在感染的巨噬细胞中倾向于坏死而不是凋亡，这被认为是逃避宿主免疫反应的一种机制。我们最近报道，可以在结核病患者的血液细胞中观察到与这一假设一致的效应，在本文中，我们回顾了有关结核分枝杆菌采用的逃避策略的已知情况，特别是考虑了结核分枝杆菌感染的细胞凋亡抑制效应与另一种因子(IL-4)的可能相互作用，IL-4的表达被认为在控制结核杆菌感染的失败中发挥了作用。已有研究指出，IL-4可加重肿瘤坏死因子-α诱导的病理改变，但其机制尚不清楚。由于结核的病理通常涉及感染细胞周围的炎性聚集，而肿瘤坏死因子-α在其中起重要作用，我们预测IL-4将通过由肿瘤坏死因子-α激活的外部途径，通过感染细胞的凋亡来抑制细胞清除结核杆菌的能力。在IL-4存在的情况下，体外用分枝杆菌感染人单核细胞，似乎促进了感染细胞的坏死而不是凋亡--这一发现与其在结核分枝杆菌感染过程中作为一个病理因素所起的作用一致。
It has been clearly demonstrated that in vitro, virulent M. tuberculosis can favor necrosis over apoptosis in infected macrophages, and this has been suggested as a mechanism for evading the host immune response. We recently reported that an effect consistent with this hypothesis could be observed in cells from the blood of TB patients, and in this paper, we review what is known about evasion strategies employed by M. tuberculosis and in particular consider the possible interaction of the apoptosis-inhibiting effects of M. tuberculosis infection with another factor (IL-4) whose expression is thought to play a role in the failure to control M. tuberculosis infection. It has been noted that IL-4 may exacerbate TNF-α-induced pathology, though the mechanism remains unexplained. Since pathology in TB typically involves inflammatory aggregates around infected cells, where TNF-α plays an important role, we predicted that IL-4 would inhibit the ability of cells to remove M. tuberculosis by apoptosis of infected cells, through the extrinsic pathway, which is activated by TNF-α. Infection of human monocytic cells with mycobacteria in vitro, in the presence of IL-4, appears to promote necrosis over apoptosis in infected cells—a finding consistent with its suggested role as a factor in pathology during M. tuberculosis infection.
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影响因子：
4.4
作者：
Demissie, A;Abebe, M;Doherty, TM
通讯作者：
Doherty, TM
影响因子：
3.7
作者：
Dasgupta A;Sureka K;Mitra D;Saha B;Sanyal S;Das AK;Chakrabarti P;Jackson M;Gicquel B;Kundu M;Basu J
通讯作者：
Basu J
影响因子：
3.1
作者：
da Fonseca, Denise Morais;Silva, Celio Lopes;Deperon Bonato, Vania Luiza
通讯作者：
Deperon Bonato, Vania Luiza
影响因子：
3.1
作者：
Briken V;Miller JL
通讯作者：
Miller JL
影响因子：
3.7
作者：
Danelishvili L;Yamazaki Y;Selker J;Bermudez LE
通讯作者：
Bermudez LE