American journal of reproductive immunology (New York, N.Y. : 1989) · 2021
Extracellular superoxide produced by Enterococcus faecalis reduces endometrial receptivity via inflammatory injury.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zhang Zhanhu, Li Tianqi, Xu Lili, Wang Qiuhong, Li Haibo, Wang Xingmin
Аннотация
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.
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.