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COPB1-knockdown induced type I interferon signaling activation inhibits Chlamydia psittaci intracellular

Nana Li1,2, Huiying Yang2,3, Shan Zhang2

  • 1Department of Epidemiology and Health Statistics, School of Public Health, Anhui Medical University, Hefei, China.

Frontiers in Microbiology
|March 21, 2025
PubMed
Abstract

Insights

Chlamydia psittaci infection relies on host cell membrane trafficking. Targeting COPI subunits, like COPB1, inhibits pathogen survival by disrupting STING protein localization and activating immune signaling.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Chlamydia psittaci is a zoonotic bacterium causing psittacosis.
  • Chlamydia species hijack host cell membrane trafficking for infection.

Purpose of the Study:

  • To identify host proteins involved in Chlamydia psittaci infection.
  • To elucidate the role of membrane trafficking in Chlamydia psittaci pathogenesis.

Main Methods:

  • Screening of a human membrane trafficking siRNA library.
  • Utilizing fluorescently labeled Chlamydia psittaci in HeLa cells.
  • Gene knockdown (KD) of identified host proteins.

Main Results:

  • 34 host proteins influencing C. psittaci infection were identified.
  • Knockdown of coatomer complex I (COPI) subunits inhibited intracellular survival.
  • COPB1 knockdown reduced C. psittaci proliferation and disrupted STING homeostasis, activating type I interferon signaling.

Conclusions:

  • Coatomer complex I (COPI) is crucial for Chlamydia psittaci intracellular survival.
  • COPB1-mediated disruption of STING-ER/Golgi trafficking activates type I interferon response.
  • Findings offer potential targets for anti-Chlamydia psittaci therapies.
Keywords:
COPB1Chlamydia psittaciGolgiSTINGtype I interferon

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