Nystatin enhances the immune response against Candida albicans and protects the ultrastructure of the vaginal epithelium in a rat model of vulvovaginal candidiasis.
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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制霉菌素增强外阴阴道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
DOI：
10.1186/s12866-018-1316-3
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发表时间：
2018-10-25
期刊：
影响因子：
4.2
通讯作者：
Liu Z
中科院分区：
文献类型：
--
作者：
Zhang X;Li T;Chen X;Wang S;Liu Z
外阴阴道念珠菌病(VVC)是一种常见的下生殖道传染病。制霉菌素是一种多烯类抗真菌抗生素，用于治疗VVC的局部抗真菌药物。本研究旨在探讨制霉菌素对白色念珠菌感染时阴道黏膜免疫应答的可能调节作用，并探讨其对阴道上皮细胞超微结构的保护作用。感染白念珠菌后，血管内皮细胞中干扰素-γ和IL-17水平显著升高，而抗体水平显著降低(P <； )。IL-4表达差异无统计学意义。制霉菌素治疗后，干扰素-γ、IL-17和免疫球蛋白水平较未治疗组显著升高(P <； 0.05)。透射电子显微镜显示，白色念珠菌通过诱导内吞和主动穿透两种方式侵入阴道上皮。制霉菌素治疗可保护阴道上皮的超微结构。与未治疗组相比，制霉菌素治疗后血管内皮细胞线粒体损伤的Flameng评分显著降低(P <； 0.001)，黏附性和侵袭性白色念珠菌数量显著减少(P <； 0.01)。制霉菌素通过上调干扰素-γ相关的细胞反应和IL-17信号通路，可能通过增强血管内皮细胞衍生的免疫球蛋白介导的免疫，在白念珠菌的宿主防御中发挥保护作用。此外，制霉菌素显著改善阴道粘膜的超微结构，部分是通过保护血管内皮细胞线粒体超微结构和抑制白色念珠菌的黏附和侵袭。总之，这些作用增强了阴道黏膜对白色念珠菌的免疫反应，并保护了VVC大鼠阴道上皮的超微结构。
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.
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