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Chlamydia trachomatis Pgp3 protein regulates oxidative stress via activation of the Nrf2/NQO1 signal pathway

Mingyi Shu1, Wenbo Lei1, Shengmei Su1

  • 1Institute of Pathogenic Biology, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang 421001, China.

Life Sciences
|April 23, 2021
PubMed
Abstract

Insights

Chlamydia trachomatis virulence factor Pgp3 alleviates host cell oxidative stress by activating the Nrf2/NQO1 pathway, enhancing bacterial survival and infectivity. This study reveals a novel mechanism in C. trachomatis pathogenesis.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Chlamydia trachomatis employs strategies to counteract host cell oxidative stress for intracellular survival.
  • The precise anti-oxidative mechanisms of C. trachomatis remain incompletely understood.
  • The nuclear factor erythroid 2-related factor 2/quinone oxidoreductase (Nrf2/NQO1) pathway is a key host defense against oxidative stress.

Purpose of the Study:

  • To investigate the role of the C. trachomatis virulence factor Pgp3 in modulating the host Nrf2/NQO1 signaling pathway.
  • To determine how Pgp3 influences host cell oxidative stress responses and bacterial survival.

Main Methods:

  • HeLa cells were stimulated with Pgp3 protein.
  • Nrf2 localization and C. trachomatis inclusion bodies were assessed via indirect immunofluorescence.
  • Western blotting and oxidative stress assay kits measured protein expression and levels of malondialdehyde (MDA), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC).
  • Nrf2 and NQO1 interference was performed to assess pathway inhibition.

Main Results:

  • Pgp3 facilitated Nrf2 nuclear translocation, upregulating NQO1 expression.
  • Pgp3 reduced lipopolysaccharide (LPS)-induced oxidative stress, promoting C. trachomatis survival.
  • Inhibition of the Nrf2/NQO1 pathway via Nrf2 inhibitor or siRNA-NQO1 diminished Pgp3-mediated oxidative stress resistance.

Conclusions:

  • Pgp3 alleviates oxidative stress in host cells by activating the Nrf2/NQO1 signaling pathway.
  • This activation enhances the infectivity and intracellular survival of C. trachomatis.
  • The findings offer new insights into the role of Pgp3 in C. trachomatis pathogenesis.
Keywords:
Chlamydia trachomatisNrf2/NQO1 signal pathwayOxidative stressPgp3 protein

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