Impaired PRR expression modulates inflammation-triggered oxidative stress and pathogenesis of recurrent vulvovaginal infections

Abstract

Introduction: Both inflammation and oxidative stress (OS) stimulate each other and act together in providing defense against recurrent vulvovaginal infections (RVVI). Both processes are in such a tight link, that defect in one may lead to defect in other; therefore, recognition and treatment of primary anomaly are of great clinical importance. Objective: To investigate the relationship between PRRs, i.e., mannose-binding lectin (MBL) and dendritic cell-associated C-type lectin-1 (Dectin-1) and oxidative stress parameters, i.e., total antioxidant status (TAC), total oxidant status (TOS), and oxidative stress index (OSI), along with their dependency on system factors in modulating susceptibility to RVVI. Study design: This case-control study included 258 RVVI cases and 203 age-matched controls. TAC, TOS, and OSI were determined according to modified standard protocols. MBL and Dectin-1 levels were assessed by commercially available kits. Results: RVVI and bacterial vaginosis showed significantly low TAC than controls. Significantly low TOS was observed in cases than controls. RVVI and vulvovaginal candidiasis showed significantly low OSI than controls. Significantly low MBL and high Dectin-1 levels were observed in cases than controls. Significant, but unexpected weak relationship, was observed between OS parameters and PRRs. Serum biomarkers were found to be dependent on confounding variables. Conclusion: Low MBL levels were found to be the primary source of defect in the present study that leads to the dysregulated immune system with no observed protective oxidative stress, increasing susceptibility to RVVI. Therefore, substituting the required MBL in representative Indian population may restore host homeostasis and provide recovery from RVVI.

Immunopathology of Recurrent Vulvovaginal Infections: New Aspects and Research Directions

“…Reduced vaginal concentrations of NO metabolites were shown to increase susceptibility to recurrent episodes of VVC (205). Likewise, reduced serum concentration of ROS has been shown to increase susceptibility to RVVI (206). Other than neutrophils, macrophages were also shown to release cytotoxic NO products against T. vaginalis with increased iNOS expression (165, 207).…”