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<p><i>Chlamydia psittaci</i> is an obligate intracellular zoonotic pathogen that causes atypical pneumonia. Pyroptosis is a type of regulated cell death mediated by gasdermin-family proteins and plays an important role in the response to intracellular infection. This study investigates whether <i>C. psittaci</i> infection triggers GSDME-mediated pyroptosis through the ROS-JNK signaling pathway. Our study revealed that infection with <i>C. psittaci</i> induces pyroptosis through caspase-3 activation and subsequent GSDME cleavage in human cervical epithelial (HeLa) cells. Mechanistically, the infection increased intracellular levels of reactive oxygen species (ROS) and phosphorylated c-Jun N-terminal kinase (JNK). Treatment with either the ROS scavenger NAC or the JNK inhibitor SP600125 significantly suppressed pyroptosis. Furthermore, inhibition of either the caspase-3-GSDME axis or the ROS-JNK pathway significantly increased the number of <i>C. psittaci</i> inclusion bodies. Taken together, our findings suggest that the ROS/JNK signaling pathway modulates GSDME-mediated pyroptosis and concurrently restricts <i>C. psittaci</i> replication in host cells, identifying the ROS-JNK-GSDME axis as a key mechanism in <i>C. psittaci</i>-induced pyroptosis. These findings reveal novel therapeutic targets for the treatment of psittacosis.</p>

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Chlamydia psittaci induces GSDME-mediated pyroptosis via the ROS-JNK signaling pathway

  • 期刊论文

  • 发表日期：

    2026年7月4日

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  • Cui Xiao,
  • Canming Hu,
  • Zhe Liu,
  • Gang Wang,
  • Chuan Wang,
  • Zhongyu Li,
  • Qinqin Bai,
  • Shenghua Chen,
  • Lili Chen

摘要

Chlamydia psittaci is an obligate intracellular zoonotic pathogen that causes atypical pneumonia. Pyroptosis is a type of regulated cell death mediated by gasdermin-family proteins and plays an important role in the response to intracellular infection. This study investigates whether C. psittaci infection triggers GSDME-mediated pyroptosis through the ROS-JNK signaling pathway. Our study revealed that infection with C. psittaci induces pyroptosis through caspase-3 activation and subsequent GSDME cleavage in human cervical epithelial (HeLa) cells. Mechanistically, the infection increased intracellular levels of reactive oxygen species (ROS) and phosphorylated c-Jun N-terminal kinase (JNK). Treatment with either the ROS scavenger NAC or the JNK inhibitor SP600125 significantly suppressed pyroptosis. Furthermore, inhibition of either the caspase-3-GSDME axis or the ROS-JNK pathway significantly increased the number of C. psittaci inclusion bodies. Taken together, our findings suggest that the ROS/JNK signaling pathway modulates GSDME-mediated pyroptosis and concurrently restricts C. psittaci replication in host cells, identifying the ROS-JNK-GSDME axis as a key mechanism in C. psittaci-induced pyroptosis. These findings reveal novel therapeutic targets for the treatment of psittacosis.