Exosomes From Adipose-Derived Stem Cells Suppress the Progression of Chronic Endometritis

Chronic endometritis (CE) is closely linked to the reproductive failure. Exosome (Exo)-based therapy is proposed as an encouraging strategy in inflammation-related disorders; however, little work has been devoted to its usage in CE therapy. An in vitro CE was established by administration of lipopolysaccharide (LPS) in human endometrial stromal cells (HESCs). The cell proliferation, cell apoptosis, and inflammatory cytokine assays were performed in vitro, and the efficacy of Exos derived from adipose tissue-derived stem cells (ADSCs) was evaluated in a mouse model of CE. We found that Exos isolated from ADSCs could be taken up by HESCs. Exos elevated the proliferation and inhibited apoptosis in LPS-treated HESCs. Administration of Exos to HESCs suppressed the content of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-1 beta (IL-1 beta). Moreover, Exos exposure repressed the inflammation stimulated by LPS in vivo. Mechanistically, we demonstrated that Exos exerted their ant-inflammatory effect via miR-21/TLR4/NF-kB signaling pathway in endometrial cells. Our findings suggest that ADSC-Exo-based therapy might serve as an attractive strategy for the treatment of CE.

Automated summary

Chronic endometritis (CE) is strongly associated with reproductive failure. Exosome-based therapy shows promise in inflammation-related disorders, but its use in CE therapy is limited. In this study, an in vitro CE model was established using lipopolysaccharide (LPS) in human endometrial stromal cells (HESCs). Exosomes from adipose tissue-derived stem cells (ADSCs) were found to enhance cell proliferation and suppress apoptosis in LPS-treated HESCs. Exosomes also decreased the levels of inflammatory cytokines TNF-alpha, IL-6, and IL-1 beta. Furthermore, Exos exposure reduced inflammation in a mouse model of CE. Mechanistically, the anti-inflammatory effects of Exos were mediated through the miR-21/TLR4/NF-kB signaling pathway. These findings suggest that ADSC-Exo-based therapy could be a promising strategy for treating CE.