Chlamydia inhibit host cell apoptosis by inducing Bag-1 via the MAPK/ERK survival pathway
Chlamydia inhibit host cell apoptosis by inducing Bag-1 via the MAPK/ERK survival pathway
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DOI：
10.1007/s10495-013-0865-z
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发表时间：
2013-09-01
期刊：
影响因子：
7.2
通讯作者：
Li Qi
中科院分区：
文献类型：
--
作者：
Du Kun;Cheng Xiang-lin;Li Qi
衣原体是经常引起人类疾病的专性细胞内细菌。感染衣原体的宿主细胞对多种细胞凋亡刺激具有很强的抵抗力。细胞凋亡的抑制被认为是一种重要的免疫逃逸机制，使衣原体能够有效地完成其专性细胞内生长周期。衣原体抗凋亡活性涉及 MAPK/ERK 存活途径的激活。然而，其分子机制尚不清楚。在这里，我们发现 Bag-1 在衣原体感染的细胞中上调。 U0126 和 GW5074 抑制衣原体对 Bag-1 的诱导，这意味着衣原体可能通过 MAPK/ERK 存活途径上调 Bag-1。 Bag-1 的过度表达足以防止细胞凋亡，而 Bag-1 的耗竭会抑制衣原体的抗细胞凋亡作用。数据表明衣原体可能通过 MAPK/ERK 存活途径上调 Bag-1 来抑制细胞凋亡。
Chlamydia are obligate intracellular bacteria that frequently cause human disease. Host cells infected with Chlamydia are profoundly resistant to diverse apoptotic stimuli. The inhibition of apoptosis is thought to be an important immune escape mechanism allowing Chlamydia to productively complete their obligate intracellular growth cycle. Chlamydial antiapoptotic activity involves activation of the MAPK/ERK survival pathway. However, the molecular mechanisms are not well understood. Here we show that Bag-1 is up-regulated in Chlamydia-infected cells. U0126 and GW5074 suppress the induction of Bag-1 by Chlamydia, implying that Chlamydia may up-regulate Bag-1 via the MAPK/ERK survival pathway. Overexpression of Bag-1 is sufficient to protect against apoptosis, while depletion of Bag-1 suppresses the antiapoptotic effect of Chlamydia. The data indicate Chlamydia may up-regulate Bag-1 through the MAPK/ERK survival pathway to suppress apoptosis.