Chronic
endometritis has a high incidence in infertile women, which is caused by endometrial microbiome
infection. In response to microbial
infection, the role of
defensins during chronic
endometritis need explored. Besides, the expression of
estrogen and its receptors vary in different menstrual cycles, but their roles in chronic
endometritis are still unclear. In this study, we used the human endometrial tissues to examine the expression of
antimicrobial peptides (AMPs) α-
defensin hNP-1 and β-
defensins hBD-1, hBD-2, hBD-3, hBD-4 and LCN2. We found the expression of hBD-1 and LCN2 were downregulated in
endometritis tissues, while the expressions of hBD-2, hBD-3, hBD-4,
hNP-1, and
estrogen and ERα were upregulated in chronic
endometritis tissues compared to normal tissues. The expression and phosphorylation of
STING, which is a crucial mediator of mammalian innate immunity in response to pathogens, was regulated with the treatment of ERα inhibitor
raloxifene (Rx). Furthermore, using with the
estrogen receptor inhibitor Rx and
STING inhibitor H-151 significantly decreases the LCN2 expression. Taken together, these results suggested ERα was upregulated to modulate
STING expression inducing LCN2
antimicrobial peptide expression to modulate the mucosal immunity during chronic
endometritis.