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<p>Vulvovaginal candidiasis (VVC) and recurrent vulvovaginal candidiasis (RVVC) are among the most common infections of the lower genital tract in reproductive-age women. While host immune mechanisms have garnered increasing attention in these infections, the specific underlying mechanisms remain poorly understood. In this study, we compared the immune responses between VVC and RVVC, investigating the immune mechanisms by which <i>Candida albicans</i> affects the host. We established RVVC mouse models using <i>Candida albicans</i> derived from both VVC and RVVC infections, and assessed changes in infection rates, vaginal epithelial histopathology, and inflammation. Additionally, we infected VK2 human vaginal epithelial cells with <i>Candida albicans</i> for RNA sequencing and established a cell model. To explore the underlying mechanisms, we intervened with an NLRP3 inhibitor and performed qPCR, Western blot, and immunofluorescence staining to evaluate the expression of NLRP3 and IL-1β. Moreover, we assessed the expression of pro-IL-1β, cleaved caspase-1, GSDMD-NT, and ASC proteins, and conducted PI staining to evaluate changes in membrane permeability and cell injury. Our results showed that <i>Candida albicans</i>-induced changes in IL-1β were associated with both VVC and RVVC, suggesting that NLRP3-mediated IL-1β secretion may contribute to in modulating host immune responses. Notably, PI staining demonstrated an increased proportion of PI-positive cells, and protein analyses showed elevated expression of ASC, cleaved caspase-1, and GSDMD-NT, consistent with inflammasome activation and increased membrane permeability. Compared with the VVC group, epithelial damage was partially alleviated in the RVVC group, although epithelial thickness remained higher than that in the control group.In conclusion, this study suggests that NLRP3/IL-1β-mediated inflammation is associated with the host immune response in both VVC and RVVC. The increased expression of inflammasome-associated proteins, together with increased PI-positive cells, suggests enhanced membrane permeability and inflammasome-associated cell injury following <i>Candida albicans</i> infection. These findings provide new insights into the inflammatory mechanisms underlying these infections.</p>

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The pathogenic Candida albicans regulates local vaginal epithelial immunity through the NLRP3/IL-1β pathway in VVC/RVVC mouse models

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月26日

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  • Xiaoyan Wang,
  • Rujia Qin,
  • Yuhui Mao,
  • Changju Li,
  • Congrong Yang,
  • Mingsheng Ma

摘要

Vulvovaginal candidiasis (VVC) and recurrent vulvovaginal candidiasis (RVVC) are among the most common infections of the lower genital tract in reproductive-age women. While host immune mechanisms have garnered increasing attention in these infections, the specific underlying mechanisms remain poorly understood. In this study, we compared the immune responses between VVC and RVVC, investigating the immune mechanisms by which Candida albicans affects the host. We established RVVC mouse models using Candida albicans derived from both VVC and RVVC infections, and assessed changes in infection rates, vaginal epithelial histopathology, and inflammation. Additionally, we infected VK2 human vaginal epithelial cells with Candida albicans for RNA sequencing and established a cell model. To explore the underlying mechanisms, we intervened with an NLRP3 inhibitor and performed qPCR, Western blot, and immunofluorescence staining to evaluate the expression of NLRP3 and IL-1β. Moreover, we assessed the expression of pro-IL-1β, cleaved caspase-1, GSDMD-NT, and ASC proteins, and conducted PI staining to evaluate changes in membrane permeability and cell injury. Our results showed that Candida albicans-induced changes in IL-1β were associated with both VVC and RVVC, suggesting that NLRP3-mediated IL-1β secretion may contribute to in modulating host immune responses. Notably, PI staining demonstrated an increased proportion of PI-positive cells, and protein analyses showed elevated expression of ASC, cleaved caspase-1, and GSDMD-NT, consistent with inflammasome activation and increased membrane permeability. Compared with the VVC group, epithelial damage was partially alleviated in the RVVC group, although epithelial thickness remained higher than that in the control group.In conclusion, this study suggests that NLRP3/IL-1β-mediated inflammation is associated with the host immune response in both VVC and RVVC. The increased expression of inflammasome-associated proteins, together with increased PI-positive cells, suggests enhanced membrane permeability and inflammasome-associated cell injury following Candida albicans infection. These findings provide new insights into the inflammatory mechanisms underlying these infections.