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首页> 外文期刊>American Journal of Veterinary Research >The Chlamydia trachomatis Inclusion Membrane Protein CpoS Counteracts STING-Mediated Cellular Surveillance and Suicide Programs
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The Chlamydia trachomatis Inclusion Membrane Protein CpoS Counteracts STING-Mediated Cellular Surveillance and Suicide Programs

机译：Chlamydia Thachomatis包涵体蛋白CPOS抵消了刺痛介导的细胞监测和自杀计划

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摘要

Evading cell death is critical for Chlamydia to maintain a replicative niche, but the underlying mechanisms are unknown. We screened a library of Chlamydia mutants for modulators of cell death. Inactivation of the inclusion membrane protein CpoS (Chlamydia promoter of survival) induced rapid apoptotic and necrotic death in infected cells. The protection afforded by CpoS is limited to the inclusion in which it resides, indicating that it counteracts a spatially restricted pro-death signal. CpoS-deficient Chlamydia induced an exacerbated type I interferon response that required the host cGAS/STING/TBK1/IRF3 signaling pathway. Disruption of STING, but not cGAS or IRF3, attenuated cell death, suggesting that STING mediates Chlamydia-induced cell death independent of its role in regulating interferon responses. CpoS-deficient strains are attenuated in their ability to propagate in cell culture and are cleared faster from the murine genital tract, highlighting the importance of CpoS for Chlamydia pathogenesis.
机译：逃避细胞死亡对于维持复制的利基而言，衣原体至关重要，但潜在的机制是未知的。我们筛选了一种用于细胞死亡的调节剂的衣原体突变体。纳入膜蛋白CPOS（存活的衣原体启动子）灭活诱导感染细胞中快速的凋亡和坏死性死亡。 CPO提供的保护仅限于它所存在的夹杂物，表明它抵消了空间限制的前死亡信号。 CPOS缺陷型衣原体诱导加剧I型Interferon响应，所以需要宿主CGA / Sting / TBK1 / IRF3信号通路。刺痛的破坏，但不是CGA或IRF3，减毒细胞死亡，表明Sting介导衣原体诱导的细胞死亡，独立于其在调节干扰素反应方面的作用。 CPOS缺陷的菌株在其在细胞培养中繁殖的能力中衰减，并且从鼠生殖道中清除速度更快，突出了CPO对衣原体发病机制的重要性。

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