Gut dysbiosis contributes to chlamydial induction of hydrosalpinx in the upper genital tract.

Abstract

Chlamydia trachomatis is one of the most common sexually infections that cause infertility, and its genital infection induces tubal adhesion and hydrosalpinx. Intravaginal Chlamydia muridarum infection in mice can induce hydrosalpinx in the upper genital tract and it has been used for studying C. trachomatis pathogenicity. DBA2/J strain mice were known to be resistant to the chlamydial induction of hydrosalpinx. In this study, we took advantage of this feature of DBA2/J mice to evaluate the role of antibiotic induced dysbiosis in chlamydial pathogenicity. Antibiotics (vancomycin and gentamicin) were orally administrated to induce dysbiosis in the gut of DBA2/J mice. The mice with or without antibiotic treatment were evaluated for gut and genital dysbiosis and then intravaginally challenged by C. muridarum. Chlamydial burden was tested and genital pathologies were evaluated. We found that oral antibiotics significantly enhanced chlamydial induction of genital hydrosalpinx. And the antibiotic treatment induced severe dysbiosis in the GI tract, including significantly reduced fecal DNA and increased ratios of firmicutes over bacteroidetes. The oral antibiotic did not alter chlamydial infection or microbiota in the mouse genital tracts. Our study showed that the oral antibiotics-enhanced hydrosalpinx correlated with dysbiosis in gut, providing the evidence for associating gut microbiome with chlamydial genital pathogenicity.