Description
Impact of semen exposure on cytokine response and bacterial vaginosis in the female genital tract
Khanyisile Mngomezulu1, Cheryl Baxter1, Andile Mtshali1, Lenine Liebenberg1,2, Nigel Garrett1, Sinaye Ngcapu1,2
1Centre for the AIDS Programme of Research in South Africa (CAPRISA), Nelson Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa; 2Department of Medical Microbiology, University of KwaZulu-Natal, Durban, South Africa
Diverse microbial communities and inflammatory cytokine responses in the lower female genital tract (FGT) are closely associated with increased HIV risk, possibly through increasing mucosal HIV target cell frequency and T-cell activation. The presence of semen in the vagina during unprotected sex has been associated with short-term activation of mucosal immunity. Here, we investigated the extent to which partner semen impacts on cytokine and microbial profiles measured in 248 HIV-uninfected women at high risk for HIV infection. We assessed the semen exposure in SoftCup supernatants by quantifying prostate specific antigen (PSA) levels using ELISA. Luminex was used to measure 48 cytokines in SoftCup supernatants and the vaginal swabs were used for diagnosis of bacterial vaginosis by Nugent score. PSA, which denotes semen exposure within 48 hours prior to sampling, was detected in 19% (43/248) of SoftCup supernatants. Of the 43 PSA positive women, 70% (30/43) had self-reported condom use at their last sex act and 84% (36/43) had non-Lactobacillus dominant microbiota (Nugent score >7). In addition, PSA was significantly associated with prevalent bacterial vaginosis (Relative Risk (RR), 2.609; 95% Confidence Interval (CI), 1.104 - 6.165; p = 0.029), after adjusting for potential confounders such as age, STIs, current contraceptive use and condom use. Furthermore, women with detectable PSA had high median concentrations of MIP-1β (p=0.047) compared to those without PSA. These findings suggest that the presence of semen have a potential to alter the inflammatory response and microbial communities of the FGT, which may facilitate recruitment of HIV susceptible cells, resulting in increased susceptibility to HIV-1 infection.