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Extracellular superoxide produced by Enterococcus faecalis reduces endometrial receptivity via inflammatory injury
Author(s) -
Zhang Zhanhu,
Li Tianqi,
Xu Lili,
Wang Qiuhong,
Li Haibo,
Wang Xingmin
Publication year - 2021
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.13453
Subject(s) - enterococcus faecalis , superoxide , endometritis , endometrium , microbiology and biotechnology , andrology , biology , medicine , immunology , staphylococcus aureus , bacteria , biochemistry , pregnancy , genetics , enzyme
Problem Chronic endometritis (CE) can cause infertility. Enterococcus faecalis is an opportunistic pathogen that is often found in the endometrium of CE patients. However, the mechanisms by which E . faecalis affects endometrial health are still unclear. In this study, we investigated the mechanism how extracellular superoxide produced by E . faecalis affected the endometrial receptivity. Method of Study Superoxide production was blocked by deleting menB gene in E . faecalis OG1RF. Endometrial epithelial cells were infected by superoxide‐producing E . faecalis OG1RF and superoxide‐deficient strain WY84. Inflammatory cytokines, apoptosis, and biomarkers for the endometrial receptivity were analyzed. Results Infection of endometrial epithelial cells with superoxide‐producing E . faecalis OG1RF induced expression of inflammatory cytokines, promoted apoptosis, and down‐regulated expression of receptivity biomarkers compared to uninfected control. In contrast, superoxide‐deficient E . faecalis WY84 had little effect on inflammatory cytokine production, apoptosis, and endometrial receptivity biomarkers. Conclusions Extracellular superoxide produced by E . faecalis is an important virulence factor for E . faecalis ‐induced endometritis leading to reduced receptivity of endometrial epithelial cells.