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Chlamydia trachomatis plasmid-encoded protein pORF5 protects mitochondrial function by inducing mitophagy and increasing HMGB1 expression.

Research paper by Wenbo W Lei, Qun Q Li, Shengmei S Su, Jichang J Bu, Qiulin Q Huang, Zhongyu Z Li

Indexed on: 19 Oct '17Published on: 19 Oct '17Published in: Pathogens and Disease



Abstract

Chlamydia trachomatis, an obligate intracellular pathogen, has various effective strategies to regulate host cell death signalling pathways that ensure completion of their growth cycle. Mitochondrial autophagy (mitophagy) is responsible for elimination of dysfunctional and impaired mitochondria, and this process plays a critical role in cell survival via restriction of the mitochondrial apoptotic pathway. However, the specific molecular mechanisms are not entirely understood. In the present study, we observed that pORF5 plasmid protein of C. trachomatis plays a crucial role in attenuating mitochondrial dysfunction and apoptosis. Knockdown high mobility group box 1 (HMGB1) by lentivirus suppressed pORF5-induced mitophagy and increased apoptosis, implying that pORF5 may participate in cell death signalling pathways via up-regulation of HMGB1. Thus, we concluded that up-regulation of HMGB1 is a pivotal event for C. trachomatis that manipulates mitophagy and apoptosis in order to establish a favourable environment supportive of Chlamydial growth, which should further promote our understanding of Chlamydial pathogenic mechanisms.