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首页> 外文期刊>BMC Microbiology >Nystatin enhances the immune response against Candida albicans and protects the ultrastructure of the vaginal epithelium in a rat model of vulvovaginal candidiasis
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Nystatin enhances the immune response against Candida albicans and protects the ultrastructure of the vaginal epithelium in a rat model of vulvovaginal candidiasis

机译：制霉菌素增强外阴念珠菌病大鼠模型中针对白色念珠菌的免疫反应并保护阴道上皮的超微结构

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Vulvovaginal candidiasis (VVC) is a common infectious disease of the lower genital tract. Nystatin, a polyene fungicidal antibiotic, is used as a topical antifungal agent for VVC treatment. The aim of the current study was to investigate the possible immunomodulatory effects of nystatin on the vaginal mucosal immune response during Candida albicans infection and examine its role in protection of vaginal epithelial cell (VEC) ultrastructure. Following infection with C. albicans, IFN-γ and IL-17 levels in VECs were significantly elevated, while the presence of IgG was markedly decreased as compared to uninfected controls (P   0.05). No significant differences in IL4 expression were observed. After treatment with nystatin, the level of IFN-γ, IL-17 and IgG was dramatically increased in comparison to the untreated group (P   0.05). Transmission electron microscopy revealed that C. albicans invades the vaginal epithelium by both induced endocytosis and active penetration. Nystatin treatment protects the ultrastructure of the vaginal epithelium. Compared with the untreated C. albicans-infected group, Flameng scores which measure mitochondrial damage of VECs were markedly decreased (P   0.001) and the number of adhesive and invasive C. albicans was significantly reduced (P   0.01) after treatment with nystatin. Nystatin plays a protective role in the host defense against C. albicans by up-regulating the IFN-γ-related cellular response, the IL-17 signaling pathway and possibly through enhancing VEC-derived IgG-mediated immunity. Furthermore, nystatin notably improves the ultramorphology of the vaginal mucosa, partially through the protection of mitochondria ultrastructure in VECs and inhibition of adhesion and invasion by C. albicans. Together, these effects enhance the immune response of the vaginal mucosa against C. albicans and protect the ultrastructure of vaginal epithelium in VVC rats.
机译：外阴念珠菌病（VVC）是下生殖道的常见传染病。制霉菌素（一种多烯杀真菌抗生素）被用作VVC治疗的局部抗真菌剂。本研究的目的是研究制霉菌素对白色念珠菌感染期间阴道黏膜免疫反应的可能免疫调节作用，并研究其在保护阴道上皮细胞（VEC）超微结构中的作用。与未感染的对照相比，感染白色念珠菌后，VEC中的IFN-γ和IL-17水平显着升高，而IgG的存在则明显降低（P <0.05）。没有观察到IL4表达的显着差异。用制霉菌素治疗后，与未治疗组相比，IFN-γ，IL-17和IgG的水平显着增加（P <0.05）。透射电子显微镜显示，白色念珠菌通过诱导的内吞作用和主动渗透作用侵入阴道上皮。制霉菌素治疗可以保护阴道上皮的超微结构。与未经治疗的白色念珠菌感染组相比，用制霉菌素治疗后，衡量VEC线粒体损伤的Flameng得分显着降低（P <0.001），粘附和浸润白色念珠菌的数量显着减少（P <0.01）。制霉菌素通过上调IFN-γ相关的细胞应答，IL-17信号通路并可能通过增强VEC衍生的IgG介导的免疫，在宿主抗白念珠菌中起保护作用。此外，制霉菌素部分地通过保护VEC中的线粒体超微结构以及抑制白色念珠菌的粘附和侵袭而显着改善了阴道粘膜的超形态学。这些作用共同增强了阴道黏膜对白色念珠菌的免疫反应，并保护了VVC大鼠的阴道上皮超微结构。

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