Purposes

To investigate the role of 17β-estrogen in Candida albicans (C. albicans) adhesion on human vaginal epithelial cells in vulvovaginal candidiasis (VVC).

Methods

The vaginal epithelial cell line, VK2/E6E7, was used to study the estrogen-induced molecular events between C. albicans and cells. An adhesion study was performed to evaluate the involvement of the estrogen-dependent focal adhesion kinase (FAK) activation in cell adhesion. The phosphorylation status of FAK and estrogen receptor α (ERα) upon estrogen challenge was assessed by western blotting. Specific inhibitors for ERα were used to validate the involvement of ERα–FAK signaling cascade.

Results

A transient activation of ERα and FAK was observed following the stimulation with 1000 nM estrogen for 48 h, as well as the increased average number of C. albicans adhering to each vaginal epithelial cell. Estrogen-induced activation of ERa and FAK was inhibited by the specific inhibitor of ERα, especially when the inhibitor reached a 10 μM concentration and allowed to act for 12 h. Simultaneously, a decrease in the number of adherent C. albicans was observed. However, this inhibitory effect diminished as the concentration of estrogen increased.

Conclusion

FAK and ERα signaling cascades were involved in the early interaction between the vaginal epithelial cells and C. albicans, which appeared to be linked with the enhanced cell adhesion leading to VVC and promoted by a certain concentration of estrogen.

中文翻译：

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17β-雌激素在白色念珠菌通过FAK磷酸化作用对人阴道上皮细胞的粘附中的作用。

目的

调查17β-雌激素在白色念珠菌（白色念珠菌）对人阴道念珠菌病（VVC）的人阴道上皮细胞粘附中的作用。

方法

阴道上皮细胞系VK2 / E6E7用于研究雌激素诱导的白色念珠菌与细胞之间的分子事件。进行了粘附研究，以评估雌激素依赖性局灶性粘附激酶（FAK）激活与细胞粘附的关系。通过蛋白质印迹法评估雌激素激发后FAK和雌激素受体α（ERα）的磷酸化状态。使用特定的ERα抑制剂来验证ERα–FAK信号级联反应的参与。

结果

在用1000 nM雌激素刺激48小时后，观察到ERα和FAK的瞬时激活，以及粘附在每个阴道上皮细胞上的白色念珠菌的平均数量增加。雌激素诱导的ERα和FAK的激活被ERα的特异性抑制剂抑制，特别是当该抑制剂的浓度达到10μM并允许作用12 h时。同时，观察到粘附的白色念珠菌数量减少。但是，随着雌激素浓度的增加，这种抑制作用减弱。

结论

FAK和ERα信号级联反应参与了阴道上皮细胞和白色念珠菌之间的早期相互作用，这似乎与导致VVC的细胞粘附增强有关，并被一定浓度的雌激素所促进。