Vulvovaginal candidiasis (VVC) and recurrent vulvovaginal candidiasis (RVVC) are the most common lower genital tract infections in reproductive women. In recent years, the research on its pathogenesis mainly focuses on vaginal local immunity and IL-17 as key factors in adaptive immunity, attracting much attention. However, the role of IL-17 in local immunity in VVC and RVVC is poorly understood. At the same time, neutrophils are considered the most effective way to control and eliminate candidal infection and have a controversial role in VVC and RVVC. In this study, we built a mouse RVVC model. After analyzing the vaginal lavage solution of RVVC mice with an inflammatory factor antibody chip and ELISA, we found that IL-17 may play a protective role in RVVC. The experiment of constructing RVVC mice with different concentrations of IL-17 using halofuginone and comparing the vaginal fungi load and vaginal epithelial damage verified that IL-17 had a protective effect in RVVC. In addition, in vitro and in vivo studies found that IL-17 can promote neutrophil apoptosis and recruit neutrophils in the vagina. The neutrophils in the vagina can secrete IL-17 in an autocrine manner. These two may be why IL-17 plays a protective role in RVVC. In summary, the study suggests that IL-17-mediated regulation of neutrophil function is involved in host immune response to RVVC, which helps us to further understand the potential mechanism of IL-17 in RVVC.
Background The role of fungal pathogenic factors and the immune response of the vaginal epithelium in vulvovaginal candidiasis (VVC) and recurrent vulvovaginal candidiasis (RVVC) are still unclear. Our study wants to clarify whether there are differences in pathogenic factors between VVC and RVVC strains, confirm the roles of pathogenic factors in the pathogenesis of RVVC, and analyze the influence of pathogenic factors on vaginal host immunity. Methods VVC- and RVVC-causing Candida albicans strains were genotyped with 25S rDNA. Drug susceptibility assays using a modified alamarBlue broth microdilution method were carried out. Milk culture medium and egg yolk culture medium were used to measure the secreted aspartate protease (Sap) and phospholipase (Plb) activity of the samples. We used C. albicans with different Sap activity levels to induce RVVC in mice and measured interleukin 4 (IL4), interleukin 8 (IL8), and interleukin 17 (IL17) in vaginal lavage fluid at different stages of RVVC infection. Results There were no significant differences between VVC and RVVC fungi except that the Sap activity was lower for RVVC-causing C. albicans than for VVC-causing C. albicans . C. albicans with both strong Sap and weak Sap induced RVVC in mice. C. albicans with strong Sap had a reduced RVVC infection rate. In addition, C. albicans with strong Sap stimulated the vaginal epithelium to secrete more IL4, IL8, and IL17. Conclusion Compared with that of VVC-causing C. albicans , the Sap activity of RVVC-causing C. albicans was lower. C. albicans with strong Sap was less capable of causing repeated vaginal infections than that with weak Sap and stimulated the vaginal epithelium to produce more cytokines.
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