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Browsing Statistics by Author "Baxter, Cheryl."

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    The impact of semen exposure on cytokine response and bacterial vaginosis in the female genital tract.
    (2018) Mngomezulu, Khanyisile Happiness.; Ngcapu, Sinaye.; Baxter, Cheryl.
    Background: Diverse microbial communities and inflammatory cytokine responses in the lower female genital tract (FGT) are closely associated with increased human immunodeficiency virus (HIV-1) 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. Methods: We assessed the semen exposure in SoftCup supernatants by quantifying prostate specific antigen (PSA) levels using enzyme-linked immunosorbent assay (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. Results: 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 Macrophage inflammatory protein- beta (MIP-1β) (p=0.047) compared to those without PSA. Conclusion: These findings suggest that the presence of semen has 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.