数字农科院2.0

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

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

作者机构:

关键词: Apoptosis;Cytokines;H3K9me3;IRE1/ASK1/JNK;Mycobacterium tuberculosis PE17

期刊名称: Microbial Pathogenesis

ISSN: 0882-4010

年卷期: 2021 年 159.0 卷

页码:

收录情况: JCR(2021版)

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 IL1β, IL6, TNFα, 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 IRE1α/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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