Estrogen, the predominant sex hormone, has been found to be related to the occurrence of vaginal infectious diseases. However, its role in the occurrence and development of bacterial vaginitis caused by
Escherichia coli
is still unclear. The objective of this study was to investigate the role of 17β-estrogen in
E. coli
adhesion on human vaginal epithelial cells. The vaginal epithelial cell line, VK2/E6E7, was used to study the molecular events induced by estrogen between
E. coli
and cells. An adhesion study was performed to evaluate the involvement of the estrogen-dependent focal adhesion kinase (FAK) activation with 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. The results showed that, following the stimulation with 1000 nM estrogen for 48 h, a transient activation of ERα and FAK was observed, as well as the increased average number of
E. coli
adhering to vaginal epithelial cell. In addition, 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 acted for 1 h, and a decrease in the number of adherent
E. coli
was observed simultaneously. However, this inhibitory effect diminished as the concentration of estrogen increased. In conclusion, FAK and ERα signaling cascades were assosiated with the increasing
E. coli
adherence to vaginal epithelial cells, which was promoted by a certain concentration of estrogen.
Cranberry Products Inhibit Adherence of P-Fimbriated Escherichia Coli to Primary Cultured Bladder and Vaginal Epithelial Cells
