Adherent Bacteria and Parasiticidal Secretion Products of Human Cervicovaginal Microbiota-Associated Lactobacillus gasseri Confer Non-Identical Cell Protection against Trichomonas vaginalis-Induced Cell Detachment.

Bénédicte Pradines, Séverine Domenichini, Vanessa Lievin-Le Moal
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引用次数: 2

Abstract

Trichomonas vaginalis, 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 Lactobacillus, including those of L. gasseri in particular, can counteract T. vaginalis pathogenesis, but the mechanisms involved have yet to be clarified. T. vaginalis strain G3 (Tv 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 L. gasseri ATCC 9857 and KS 120.1 on the Tv G3 viability and parasite deleterious effects on HeLa cells were investigated. Pre-adhering L. gasseri cells delayed but did not inhibit Tv G3-induced cell detachment, F-actin cytoskeleton disorganization and the disappearance of vinculin-positive focal FAs. L. gasseri KS 120.1 secretion products had a rapid parasiticide activity by killing time- and concentration-dependent Tv G3 parasites after direct contact. By killing Tv G3 parasites already associated with the epithelial cells, secretion products have abolished parasite-induced cell detachment. Our findings suggest that vagina microbiota-associated L. gasseri creates a physical barrier and exerts pharmacological-type mechanisms to counteract the deleterious cytotoxic effects of T. vaginalis.

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人宫颈阴道微生物群相关的附壁细菌和杀寄生分泌产物对阴道毛滴虫诱导的细胞脱落具有不同的细胞保护作用。
阴道毛滴虫是一种人类生殖道特有的原生寄生虫,是最常见的性传播病原体之一。它的致病性与它在宿主上皮细胞中表达的一系列引发细胞毒性作用的蛋白酶密切相关。阴道微生物群相关的乳酸菌,特别是乳杆菌,可以抵消阴道乳杆菌的发病机制,但所涉及的机制尚未明确。采用共聚焦激光扫描电镜观察宫颈阴道上皮HeLa细胞单层上的细胞形态、细胞脱离、f -肌动蛋白细胞骨架的荧光标记和血管素位置黏附(FAs)的免疫标记,评估阴道T. G3 (Tv G3)的细胞毒性。研究了细菌细胞和L. gasseri ATCC 9857和KS 120.1分泌产物对Tv G3活力的抑制作用以及寄生虫对HeLa细胞的有害作用。预黏附L. gasseri细胞延迟但不抑制Tv g3诱导的细胞脱离、f -肌动蛋白细胞骨架破坏和血管素阳性局灶FAs的消失。经直接接触,L. gasseri KS 120.1分泌产物具有快速的杀虫活性,可杀灭具有时间和浓度依赖性的Tv G3寄生虫。通过杀死已经与上皮细胞相关的Tv G3寄生虫,分泌产物消除了寄生虫诱导的细胞脱离。我们的研究结果表明,阴道微生物群相关的乳杆菌产生了物理屏障,并发挥药理学机制来抵消阴道乳杆菌的有害细胞毒性作用。
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