Chlamydia trachomatis modulates the expression of JAK-STAT signaling components to attenuate the type II interferon response of epithelial cells.

Abstract

As an obligate intracellular pathogen that has evolved to infect the genital epithelium, Chlamydia has developed strategies to prevent detection and antimicrobial signaling in its host to ensure its survival and spread. A major player in clearing Chlamydia infections is the inflammatory cytokine interferon-γ (IFNγ), which is produced by immune cells that are recruited to the site of infection. Reports of IFNγ levels in endocervical specimens from Chlamydia-infected patients range from 1 to 350 pg/mL, while most in vitro studies of the effects of IFNγ on chlamydial growth have used 15-85-fold higher concentrations. By using physiologically relevant concentrations of IFNγ, we were able to assess Chlamydia's ability to modulate its signaling. We found that Chlamydia decreases the expression of multiple components that are required for inducing gene expression by IFNγ, providing a possible mechanism by which Chlamydia trachomatis can attenuate the immune response in the female genital tract to cause long-term infections.