Host-microbe signatures of oxidative stress and epithelial apoptosis in bacterial vaginosis during pregnancy

Bacterial vaginosis (BV) is a common vaginal dysbiosis associated with adverse pregnancy outcomes. However, the extent to which microbial indicators of dysbiosis covary with host oxidative stress and epithelial apoptotic responses during pregnancy remains unclear.

In this analytical cross-sectional study, 220 pregnant women were screened at a referral gynecology clinic in Faisalabad, Pakistan; 168 met the eligibility criteria and had concordant modified Amsel and Nugent classifications (56 BV-positive, 112 BV-negative). Cervicovaginal secretions, vaginal swabs, and serum were analyzed for microbial, oxidative stress, and host-response markers. Epithelial-enriched cervicovaginal specimens passing predefined quality criteria (n = 142) were used for apoptosis-related gene expression and caspase-3/7 activity assays. Targeted microbial quantification focused on Lactobacillus and Acinetobacter spp. Associations between bacterial burden and host markers were evaluated using correlation and regression analyses with the Benjamini-Hochberg false-discovery-rate correction, where applicable.

BV-positive participants exhibited a lower Lactobacillus spp. burden and a higher Acinetobacter spp., burden than BV-negative controls. They also showed higher cervicovaginal malondialdehyde and H₂O₂ concentrations and lower superoxide dismutase and catalase activities (all FDR-adjusted q < 10^-13). Epithelial-enriched specimens from BV-positive participants demonstrated a higher BAX/BCL2 ratio, increased caspase-3/7 activity, increased expression of BAX, CASP9, CASP3, SOD2, and HMOX1, and reduced BCL2 expression. Higher Acinetobacter spp. burden covaried with greater local oxidative stress and increased epithelial apoptosis-associated signaling, although these associations were attenuated after adjustment for BV status.

BV in pregnancy was associated with concurrent differences in cervicovaginal microbial indicators, oxidative stress, and epithelial apoptosis-related responses, supporting an integrated host-microbe response at the cervicovaginal interface. These findings provide a foundation for future longitudinal and mechanistic studies investigating host-microbe interactions in pregnancy-associated BV.