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Mycoplasma ovipneumoniae induces caspase-8-dependent extrinsic apoptosis and p53- and ROS-dependent intrinsic apoptosis in murine alveolar macrophages.

PMID: 34678131 (view PubMed database entry)
DOI: 10.1080/21505594.2021.1984714 (read at publisher's website )

Jing Chen, Yi Zhou, Erpeng Zhu, Peng Yang, Mei Li, Shuangxiang Zhang, Jun Yue, Ming Wen, Kaigong Wang, Zhentao Cheng,

<i>Mycoplasma ovipneumoniae (MO)</i> is a principle causative agent of chronic respiratory disease in ruminants, including sheep, goats, and deer, posing a great threat to the ruminant industry worldwide. However, the pathogenesis of <i>MO</i> infection still remains not well understood and needs further clarification. Here we report a time-dependent apoptosis in cultured murine alveolar macrophage (MH-S) cell lines in response to <i>MO</i> infection <i>in vitro</i>. Mechanistically, <i>MO</i> infection activated apoptosis in MH-S cells through caspase-8-dependent extrinsic pathway and through tumor protein 53 (p53)- and reactive oxygen species (ROS)-dependent intrinsic mitochondrial pathways. Moreover, <i>MO</i> infection promoted both transcription and translation of proinflammatory cytokine genes including <i>interleukin-1β</i> (<i>IL-1β), IL-18</i>, and <i>tumor necrosis factor-α</i> (<i>TNF-α</i>), in a caspase-8-, p53-, and ROS-dependent manner, implying a potential link between <i>MO</i>-induced inflammation and apoptotic cell death. Collectively, our results suggest that <i>MO</i> infection induces the activation of extrinsic and intrinsic apoptotic pathways in cultured MH-S cells, which is related to upregulated expression of proinflammatory cytokines. Our findings will contribute to the elucidation of pathogenesis in <i>MO</i> infection and provide valuable reference for the development of new strategies for controlling <i>MO</i> infection.

Virulence (Virulence)
[2021, 12(1):2703-2720]

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