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Updated: Jul 6, 2026

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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.
Molecular and Cellular Biochemistry
|July 4, 2026
Summary
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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