{"title":"COPB1-knockdown induced type I interferon signaling activation inhibits <i>Chlamydia psittaci</i> intracellular proliferation.","authors":"Nana Li, Huiying Yang, Shan Zhang, Yufei Jiang, Yinhui Lin, Xiaoxiao Chen, Yuchen Zhang, Yonghui Yu, Xuan Ouyang, Yujun Cui, Yajun Song, Jun Jiao","doi":"10.3389/fmicb.2025.1566239","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong><i>Chlamydia psittaci</i> is a zoonotic pathogen that causes an acute disease known as psittacosis. To establish infection in host cells, <i>Chlamydia</i> manipulates the host cell's membrane trafficking pathways.</p><p><strong>Methods: </strong>In this study, using fluorescently labeled <i>C. psittaci</i> and screening a human membrane trafficking small interfering RNA (siRNA) library, we identified 34 host proteins that influenced <i>C. psittaci</i> infection in HeLa cells.</p><p><strong>Results: </strong>Among these, knockdown (KD) of two genes encoding subunits of the coatomer complex I (COPI) inhibited the pathogen's intracellular survival. Specifically, the knockdown of COPB1, a COPI subunit, significantly reduced the intracellular proliferation of <i>C. psittaci</i>. Mechanistically, we found that type I interferon negatively affected <i>C. psittaci</i> infection. Moreover, COPB1 KD disrupted the homeostasis of STING, preventing its retrieval from the Golgi back to the endoplasmic reticulum (ER), which in turn activated type I interferon signaling.</p><p><strong>Conclusion: </strong>Together, our findings advance the understanding of the mechanisms underlying <i>Chlamydia</i> infection and offer potential avenues for the development of new anti-<i>C. psittaci</i> strategies.</p>","PeriodicalId":12466,"journal":{"name":"Frontiers in Microbiology","volume":"16 ","pages":"1566239"},"PeriodicalIF":4.0000,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11922848/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Microbiology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.3389/fmicb.2025.1566239","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Chlamydia psittaci is a zoonotic pathogen that causes an acute disease known as psittacosis. To establish infection in host cells, Chlamydia manipulates the host cell's membrane trafficking pathways.
Methods: In this study, using fluorescently labeled C. psittaci and screening a human membrane trafficking small interfering RNA (siRNA) library, we identified 34 host proteins that influenced C. psittaci infection in HeLa cells.
Results: Among these, knockdown (KD) of two genes encoding subunits of the coatomer complex I (COPI) inhibited the pathogen's intracellular survival. Specifically, the knockdown of COPB1, a COPI subunit, significantly reduced the intracellular proliferation of C. psittaci. Mechanistically, we found that type I interferon negatively affected C. psittaci infection. Moreover, COPB1 KD disrupted the homeostasis of STING, preventing its retrieval from the Golgi back to the endoplasmic reticulum (ER), which in turn activated type I interferon signaling.
Conclusion: Together, our findings advance the understanding of the mechanisms underlying Chlamydia infection and offer potential avenues for the development of new anti-C. psittaci strategies.
期刊介绍:
Frontiers in Microbiology is a leading journal in its field, publishing rigorously peer-reviewed research across the entire spectrum of microbiology. Field Chief Editor Martin G. Klotz at Washington State University is supported by an outstanding Editorial Board of international researchers. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.