Mycobacterium tuberculosis PE17 (Rv1646) promotes host cell apoptosis via host chromatin remodeling mediated by reduced H3K9me3 occupancy

文献类型： 外文期刊

第一作者： Abo-Kadoum, M. A.

作者： Abo-Kadoum, M. A.;Assad, Mohammed;Ali, Md Kaisar;Uae, Moure;Nzaou, Stech A. E.;Gong, Zhen;Lambert, Nzungize;Xie, Jianping;Abo-Kadoum, M. A.;Eltoukhy, Adel;Eltoukhy, Adel;Assad, Mohammed;Moaaz, Asmaa;Ali, Md Kaisar

作者机构：

关键词： Mycobacterium tuberculosis PE17; Cytokines; IRE1; ASK1; JNK; Apoptosis

期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.738； 五年影响因子：3.664 ）

ISSN： 0882-4010

年卷期： 2021 年 159 卷

页码：

收录情况： SCI

摘要： Tuberculosis caused by Mycobacterium tuberculosis remains a serious global public health threat. M. tuberculosis PE and PPE proteins are closely involved in pathogen-host interaction. To explore the predicted function of the M. tuberculosis PE17 (Rv1646), we heterologously expressed PE17 in a non-pathogenic Mycobacterium smegmatis strain (Ms_PE17). PE17 can reduce the survival of M. smegmatis within macrophages associated with altering the transcription levels of inflammatory cytokines IL18, IL6, TNF alpha, and IL10 in Ms_PE17 infected macrophages through JNK signaling. Furthermore, macrophages apoptosis was increased upon Ms_PE17 infection in a caspases-dependent manner, accompanied by the activation of the Endoplasmic Reticulum stress IRE1 alpha/ASK1/ JNK signaling pathway. This can be largely interpreted by the epigenetic changes through reduced H3K9me3 chromatin occupancy post Ms_PE17 infection. To our knowledge, this is the first report that PE17 altered the macrophages apoptosis via H3K9me3 mediated chromatin remodeling.

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