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首页> 外文期刊>Infection and immunity >Persistent Chlamydia trachomatis Infection of HeLa Cells Mediates Apoptosis Resistance through a Chlamydia Protease-Like Activity Factor-Independent Mechanism and Induces High Mobility Group Box 1 Release
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Persistent Chlamydia trachomatis Infection of HeLa Cells Mediates Apoptosis Resistance through a Chlamydia Protease-Like Activity Factor-Independent Mechanism and Induces High Mobility Group Box 1 Release

机译：持久性沙眼衣原体感染Hela细胞通过衣原体蛋白酶样活性因子独立机制介导的抗凋亡作用并诱导高迁移率族框1释放

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Intracellular persistence of Chlamydia trachomatis has been implicated in the development of chronic infection that can result in pelvic inflammatory disease and tubal sterility. By inhibition of host cell apoptosis, chlamydiae have evolved a strategy to maintain the intracellular environment for replication and persistence. Both antiapoptotic host cell-derived factors and the chlamydial protease-like activity factor (CPAF) are involved in Chlamydia-mediated apoptosis resistance. Here, we show that in HeLa cells infected with gamma interferon (IFN-γ)-induced persistent C. trachomatis serovar D, the expression of CPAF is downregulated, and proapoptotic protease substrates are not cleaved. Persistent infection protected HeLa cells from apoptosis when they were exposed to staurosporine. Small-interfering RNA-mediated inhibition of myeloid cell leukemia 1 (Mcl-1) protein upregulation sensitized persistently infected cells for apoptosis. The inhibitor of apoptosis protein 2 (IAP-2) seems not to be relevant in this context because IAP-2 protein was not induced in response to IFN-γ treatment. Although apoptosis was inhibited, persistent infection caused cell membrane disintegration, as measured by the increased release of cytokeratin 18 from HeLa cells. Moreover, persistently infected cells released significantly increased amounts of high mobility group box 1 (HMGB1) protein which represents a proinflammatory damage-associated pattern molecule. The data of this study suggest that cells infected with persistent C. trachomatis are protected from apoptosis independently of CPAF but may promote chronic inflammation through HMGB1 release.
机译：沙眼衣原体的细胞内持久性与慢性感染的发展有关，这种慢性感染可导致盆腔炎和输卵管不育。通过抑制宿主细胞的凋亡，衣原体已经进化出一种策略来维持细胞内环境的复制和持久性。抗凋亡宿主细胞衍生因子和衣原体蛋白酶样活性因子（CPAF）均参与衣原体介导的凋亡抗性。在这里，我们显示，在感染了γ干扰素（IFN-γ）的持久性沙眼衣原体血清型D感染的HeLa细胞中，CPAF的表达被下调，并且促凋亡的蛋白酶底物也不会被切割。当持久性感染暴露于星形孢菌素时，可保护HeLa细胞免于凋亡。小干扰RNA介导的髓样细胞白血病1（Mcl-1）蛋白上调的抑制作用使持续感染的细胞对凋亡敏感。在这种情况下，凋亡蛋白2（IAP-2）的抑制剂似乎无关紧要，因为IAP-2蛋白并未响应IFN-γ处理而被诱导。尽管凋亡被抑制，但持续性感染会导致细胞膜解体，这是通过HeLa细胞中细胞角蛋白18释放量的增加来衡量的。此外，持续感染的细胞释放出大量增加的高迁移率族盒1（HMGB1）蛋白，该蛋白代表与炎症相关的模式分子。这项研究的数据表明，感染持续性沙眼衣原体的细胞不受CPAF保护免于凋亡，但可能通过HMGB1释放促进慢性炎症。

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