AI Article Synopsis
- Chlamydia trachomatis uses strategies to prevent host cell apoptosis, creating a safe environment for its lifecycle.
- The study focuses on the Pgp3 protein, a key virulence factor, which enhances the expression of HO-1 to inhibit apoptosis; disabling HO-1 negates Pgp3's anti-apoptotic effects.
- Research indicates that Pgp3 regulates HO-1 through the PI3K/Akt pathway, affecting Nrf2's ability to enter the nucleus, shedding light on how C. trachomatis manipulates cell death.
Article Abstract
As an obligate intracellular pathogen, Chlamydia trachomatis assumes various strategies to inhibit host cells apoptosis, thereby providing a suitable intracellular environment to ensure completion of the development cycle. In the current study, we revealed that Pgp3 protein, one of eight plasmid proteins of C. trachomatis that has been illustrated as the key virulence factor, increased HO-1 expression to suppress apoptosis, and downregulation of HO-1 with siRNA-HO-1 failed to exert anti-apoptosis activity of Pgp3 protein. Moreover, treatment of PI3K/Akt pathway inhibitor and Nrf2 inhibitor evidently reduced HO-1 expression and Nrf2 nuclear translocation was blocked by PI3K/Akt pathway inhibitor. These findings highlight that induction of HO-1 expression by Pgp3 protein is probably due to regulation of Nrf2 nuclear translocation activated by PI3K/Akt pathway, which provide clues on how C. trachomatis adjusts apoptosis.
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| http://dx.doi.org/10.1016/j.micpath.2023.106056 | DOI Listing |
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