Chlamydia trachomatis plasmid-encoding Pgp3 protein induces secretion of distinct inflammatory signatures from HeLa cervical epithelial cells

Cheong HC 1 , Cheok YY 1 , Chan YT 1 , Tang TF 1 , Sulaiman S 2 , Looi CY 3 Show all authors , Gupta R 4 , Arulanandam B 4 , Chang LY 1 , Wong WF 5

Affiliations 

  • 1 Department of Medical Microbiology, Faculty of Medicine, Universiti Malaya, 50603, Kuala Lumpur, Malaysia
  • 2 Department of Obstetrics and Gynecology, Faculty of Medicine, Universiti Malaya, 50603, Kuala Lumpur, Malaysia
  • 3 School of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, 47500, Subang Jaya, Selangor, Malaysia
  • 4 South Texas Center for Emerging Infectious Diseases, University of Texas at San Antonio, San Antonio, TX, USA
  • 5 Department of Medical Microbiology, Faculty of Medicine, Universiti Malaya, 50603, Kuala Lumpur, Malaysia. [email protected]
BMC Microbiol, 2023 Mar 04;23(1):58.
PMID: 36870960 DOI: 10.1186/s12866-023-02802-3

Abstract

BACKGROUND: Genital Chlamydia trachomatis infection is the most common bacterial sexual transmitted disease that causes severe complications including pelvic inflammatory disease, ectopic pregnancy, and infertility in females. The Pgp3 protein encoded by C. trachomatis plasmid has been speculated to be an important player in chlamydial pathogenesis. However, the precise function of this protein is unknown and thus remains to be thoroughly investigated.

METHODS: In this study, we synthesized Pgp3 protein for in vitro stimulation in the Hela cervical carcinoma cells.

RESULTS AND CONCLUSION: We showed that Pgp3 induced prominent expression of host inflammatory cytokine genes including interleukin-6 (IL-6), IL-8, tumor necrosis factor alpha-induced protein 3 (TNFAIP3), and chemokine C-X-C motif ligand 1 (CXCL1), implying a possible role of Pgp3 in modulating the inflammatory reaction in the host.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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