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Updated: Jul 6, 2026

Examination of Pyroptosis by Flow Cytometry
Published on: May 31, 2024
Chlamydia psittaci induces GSDME-mediated pyroptosis via the ROS-JNK signaling pathway
Cui Xiao1, Canming Hu1, Zhe Liu1
1Department of public health laboratory sciences, School of public health, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Abstract:
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.
Insights
Chlamydia psittaci infection triggers pyroptosis, a cell death process, via the ROS-JNK signaling pathway and GSDME activation. This pathway also limits bacterial replication, offering potential therapeutic targets for psittacosis.
Area of Science:
- Cell Biology
- Immunology
- Microbiology
Background:
- Chlamydia psittaci causes atypical pneumonia and is an obligate intracellular zoonotic pathogen.
- Pyroptosis, a programmed cell death, is crucial for combating intracellular infections.
Purpose of the Study:
- To investigate if C. psittaci infection induces GSDME-mediated pyroptosis via the ROS-JNK signaling pathway.
- To explore the role of this pathway in C. psittaci replication.
Main Methods:
- Infection of human cervical epithelial (HeLa) cells with C. psittaci.
- Assessing pyroptosis markers (caspase-3 activation, GSDME cleavage).
- Measuring reactive oxygen species (ROS) and phosphorylated JNK (JNK) levels.
- Utilizing ROS scavenger (NAC) and JNK inhibitor (SP600125).
Main Results:
- C. psittaci infection activated caspase-3 and cleaved GSDME, inducing pyroptosis.
- Infection elevated intracellular ROS and phosphorylated JNK levels.
- NAC and SP600125 treatments suppressed pyroptosis.
- Inhibiting the caspase-3-GSDME axis or ROS-JNK pathway increased C. psittaci inclusion bodies.
Conclusions:
- The ROS/JNK signaling pathway modulates GSDME-mediated pyroptosis in C. psittaci infection.
- This pathway restricts C. psittaci replication in host cells.
- The ROS-JNK-GSDME axis is a key mechanism in C. psittaci-induced pyroptosis, revealing potential therapeutic targets for psittacosis.
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