| Summary: | <i>Trichomonas vaginalis</i>, a protozoan parasite specific to the human genital tract, is one of the most common sexually transmitted pathogens. Its pathogenicity is strongly associated with its expression of a broad array of proteases triggering cytotoxic effects in host epithelial cells. Vaginal microbiota-associated <i>Lactobacillus</i>, including those of <i>L. gasseri</i> in particular, can counteract <i>T. vaginalis</i> pathogenesis, but the mechanisms involved have yet to be clarified. <i>T. vaginalis</i> strain G3 (<i>Tv</i> G3) cytotoxicity was assessed by examining cell morphology, cell detachment, and fluorescent labeling of the F-actin cytoskeleton and immunolabeling of vinculin-position focal adhesions (FAs) by confocal laser scanning electron microscopy on confluent cervicovaginal epithelial HeLa cell monolayers. The inhibitory effects of bacterial cells and secreted products of <i>L. gasseri</i> ATCC 9857 and KS 120.1 on the <i>Tv</i> G3 viability and parasite deleterious effects on HeLa cells were investigated. Pre-adhering <i>L. gasseri</i> cells delayed but did not inhibit <i>Tv</i> G3-induced cell detachment, F-actin cytoskeleton disorganization and the disappearance of vinculin-positive focal FAs. <i>L. gasseri</i> KS 120.1 secretion products had a rapid parasiticide activity by killing time- and concentration-dependent <i>Tv</i> G3 parasites after direct contact. By killing <i>Tv</i> G3 parasites already associated with the epithelial cells, secretion products have abolished parasite-induced cell detachment. Our findings suggest that vagina microbiota-associated <i>L. gasseri</i> creates a physical barrier and exerts pharmacological-type mechanisms to counteract the deleterious cytotoxic effects of <i>T. vaginalis.</i>
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