COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular proliferation
ObjectiveChlamydia 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.MethodsIn this study, using fluorescently labeled C. psittaci and screening a human membrane...
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Frontiers Media S.A.
2025-03-01
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| Series: | Frontiers in Microbiology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fmicb.2025.1566239/full |
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| author | Nana Li Nana Li Huiying Yang Huiying Yang Shan Zhang Yufei Jiang Yinhui Lin Xiaoxiao Chen Yuchen Zhang Yonghui Yu Xuan Ouyang Yujun Cui Yujun Cui Yajun Song Yajun Song Jun Jiao |
| author_facet | Nana Li Nana Li Huiying Yang Huiying Yang Shan Zhang Yufei Jiang Yinhui Lin Xiaoxiao Chen Yuchen Zhang Yonghui Yu Xuan Ouyang Yujun Cui Yujun Cui Yajun Song Yajun Song Jun Jiao |
| author_sort | Nana Li |
| collection | DOAJ |
| description | ObjectiveChlamydia 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.MethodsIn 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.ResultsAmong 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.ConclusionTogether, our findings advance the understanding of the mechanisms underlying Chlamydia infection and offer potential avenues for the development of new anti-C. psittaci strategies. |
| format | Article |
| id | doaj-art-e8ad1869cd4d4d3887e06e7bb651005b |
| institution | DOAJ |
| issn | 1664-302X |
| language | English |
| publishDate | 2025-03-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Microbiology |
| spelling | doaj-art-e8ad1869cd4d4d3887e06e7bb651005b2025-08-20T03:16:18ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2025-03-011610.3389/fmicb.2025.15662391566239COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular proliferationNana Li0Nana Li1Huiying Yang2Huiying Yang3Shan Zhang4Yufei Jiang5Yinhui Lin6Xiaoxiao Chen7Yuchen Zhang8Yonghui Yu9Xuan Ouyang10Yujun Cui11Yujun Cui12Yajun Song13Yajun Song14Jun Jiao15Department of Epidemiology and Health Statistics, School of Public Health, Anhui Medical University, Hefei, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaSchool of Public Health, Mudanjiang Medical University, Mudanjiang, Heilongjiang, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaDepartment of Epidemiology and Health Statistics, School of Public Health, Anhui Medical University, Hefei, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaDepartment of Epidemiology and Health Statistics, School of Public Health, Anhui Medical University, Hefei, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaState Key Laboratory of Pathogen and Biosecurity, Academy of Military Medicine Sciences, Beijing, ChinaObjectiveChlamydia 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.MethodsIn 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.ResultsAmong 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.ConclusionTogether, our findings advance the understanding of the mechanisms underlying Chlamydia infection and offer potential avenues for the development of new anti-C. psittaci strategies.https://www.frontiersin.org/articles/10.3389/fmicb.2025.1566239/fullChlamydia psittaciCOPB1type I interferonSTINGGolgi |
| spellingShingle | Nana Li Nana Li Huiying Yang Huiying Yang Shan Zhang Yufei Jiang Yinhui Lin Xiaoxiao Chen Yuchen Zhang Yonghui Yu Xuan Ouyang Yujun Cui Yujun Cui Yajun Song Yajun Song Jun Jiao COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular proliferation Frontiers in Microbiology Chlamydia psittaci COPB1 type I interferon STING Golgi |
| title | COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular proliferation |
| title_full | COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular proliferation |
| title_fullStr | COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular proliferation |
| title_full_unstemmed | COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular proliferation |
| title_short | COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular proliferation |
| title_sort | copb1 knockdown induced type i interferon signaling activation inhibits chlamydia psittaci intracellular proliferation |
| topic | Chlamydia psittaci COPB1 type I interferon STING Golgi |
| url | https://www.frontiersin.org/articles/10.3389/fmicb.2025.1566239/full |
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