ArticleInfection and immunity2022
Chlamydia psittaci Induces Autophagy in Human Bronchial Epithelial Cells via PERK and IRE1α, but Not ATF6 Pathway.
Article in Infection and immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- GRP78 dysregulation: A proposed molecular mechanism linking the tumor microenvironment to sepsis susceptibility in patients with cancer (Review).International journal of molecular medicine · 2026Review
- Chlamydia psittaci induces GSDME-mediated pyroptosis via the ROS-JNK signaling pathway.Molecular and cellular biochemistry · 2026Article
- Review
- From models to medicine: systematic development and evaluation of animal models forFrontiers in immunology · 2026Review
- Emerging Insights into Protein Post-Translational Modifications in Chlamydia-Host Interactions.The American journal of pathology · 2025Review
- Endoplasmic reticulum: the target of chlamydial manipulation.Archives of microbiology · 2025Review
- Review
- Autophagy: the misty lands ofFrontiers in cellular and infection microbiology · 2024Review
- MiR-184 targeting FOXO1 regulates host-cell oxidative stress induced byInfection and immunity · 2023Article
- [Type III secretory protein SINC ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives.Biomolecules · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydia psittaci is an important pathogen that causes chronic and atypical pneumonia in humans. Autophagy and the unfolded protein response (UPR) are important mechanisms for regulating the growth of infectious parasitic pathogens in living cells. Here, we explored whether C. psittaci infection induced autophagy via the UPR and the effect of these cellular responses on the survival and replication of C. psittaci in human bronchial epithelial cells (HBEs). Not only were the numbers of autophagosomes and the expression of LC3-II and Beclin1 increased following C. psittaci infection of HBEs, but also the expression of p62 (also called sequestosome-1) was downregulated. Moreover, after C. psittaci infection, the UPR and UPR sensors PERK/eIF2α and IRE1α/XBP1 were activated, but not the ATF6 pathway. When either Bip siRNA was used to block normal initiation of the UPR, or activation of the PERK and IER1α pathways was blocked with specific inhibitors GSK2606414 and 4μ8C, the level of autophagy caused by C. psittaci infection was significantly inhibited. Furthermore, blocking activation of the UPR and associated pathways significantly reduced the number of C. psittaci inclusions. Our research suggests that the UPR, via the PERK and IRE1α, but not ATF6 signaling pathways, regulates HBE-cell autophagy induced by C. psittaci infection and the replication of C. psittaci.
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