制霉菌素增强了对白念珠菌的免疫反应，并保护了阴道上皮的超微结构，在阴道假丝酵母菌病大鼠模型中。
Nystatin enhances the immune response against Candida albicans and protects the ultrastructure of the vaginal epithelium in a rat model of vulvovaginal candidiasis.
机构信息
Laboratory of Electron Microscopy, Ultrastructural Pathology Center, Peking University First Hospital, Beijing, 100034, China.
Department of Gynecology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, 100026, China.
出版信息
BMC Microbiol. 2018 Oct 25;18(1):166. doi: 10.1186/s12866-018-1316-3.
BACKGROUND
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.
RESULTS
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.
CONCLUSIONS
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.
背景
外阴阴道念珠菌病（VVC）是一种常见的下生殖道感染性疾病。制霉菌素是一种多烯类杀真菌抗生素，被用作 VVC 治疗的局部抗真菌药物。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。
结果
感染白色念珠菌后，VEC 中 IFN-γ 和 IL-17 水平明显升高，而 IgG 水平明显降低，与未感染对照组相比差异有统计学意义（P<0.05）。IL4 表达无明显差异。与未治疗组相比，制霉菌素治疗后 IFN-γ、IL-17 和 IgG 水平显著升高（P<0.05）。透射电镜显示，白色念珠菌通过诱导内吞作用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。与未治疗的白色念珠菌感染组相比，用 Flameng 评分（评估 VEC 线粒体损伤的指标）测量，制霉菌素治疗组的 VEC 线粒体损伤明显减少（P<0.001），黏附侵袭的白色念珠菌数量明显减少（P<0.01）。
结论
制霉菌素通过上调 IFN-γ 相关的细胞反应、IL-17 信号通路，可能通过增强 VEC 衍生的 IgG 介导的免疫作用，在宿主对白念珠菌的防御中发挥保护作用。此外，制霉菌素明显改善了阴道黏膜的超微形态，部分通过保护 VEC 线粒体的超微结构和抑制白色念珠菌的黏附和侵袭来实现。这些作用增强了阴道黏膜对白念珠菌的免疫反应，保护了 VVC 大鼠阴道上皮的超微结构。
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