Abstract
SummaryAs an inflammation of the endometrium, endometritis can affect fertility and lead to serious economic losses in the dairy industry. Widely found in various tissues and body fluids, exosomes and exosome micro (mi)RNAs have been shown to play an important regulatory role in the immune responses. As one of differentially expressed exosome miRNAs, miR‐218 is involved in the pathogenesis of bovine endometritis. The mechanisms of miR‐218 in regulating the release of cytokines and chemokines in endometritis, however, are poorly understood. Exosomes were isolated from bovine uterine cavity fluid and verified by transmission electron microscopy. An in vitro lipopolysaccharide‐treated cell model for bovine endometritis was then established to evaluate the correlation between exosome‐derived miR‐218 and the immune responses. We demonstrated that exosomes could be used to deliver miR‐218 from endometrial epithelial cells (EECs) into the uterine microenvironment and adjacent recipient cells to modulate local immune responses. miR‐218 packaged in the exosomes secreted from EECs acts as an inhibitor by blocking immune factors such as interleukin (IL)‐6, IL‐1β, tumour necrosis factor‐α, the chemokines macrophage inflammatory genes (MIP)‐1α and MIP‐1β to maintain the immune balance in the uterus. However, uterine inflammation altered the immunoregulatory mechanism of exosome miR‐218. MiR‐218 is a potential biomarker for the detection of endometritis. Our findings also revealed a new mechanism for the development of endometritis in cows.
Highlights
As an inflammation of the endometrium, bovine endometritis is associated with lower conception rates, increased intervals from calving to first service, and more culls for failure to conceive, leading to serious economic losses in the dairy industry (Hussain and Daniel, 1991)
Clinical endometritis is characterized by purulent (> 50% pus) uterine secretions which are detectable from the vagina after 21 days postpartum, or mucopurulent uterine secretions from the vagina after 26 days postpartum (Sheldon, et al, 2006); while subclinical endometritis is characterized by no purulent discharge from the vagina, with polymorphonuclear (PMN) > 18% in the uterine cytology samples at 21–33 days postpartum or PMN > 10% in the uterine cytology samples after 34– 47 days (Kasimanickam, et al, 2004)
Toll-like receptor 4 (TLR4)–LPS binding can lead to the activation of the nuclear factor jB (NF-jB) and mitogenactivated protein kinase (MAPK), and the NF-jB
Summary
Uterine inflammation altered the immunoregulatory mechanism of exosome miR218. As one of differentially expressed exosome miRNAs, miR-218 is involved in the pathogenesis of bovine endometritis. The mechanisms of miR-218 in regulating the release of cytokines and chemokines in endometritis, are poorly understood. Exosomes were isolated from bovine uterine cavity fluid and verified by transmission electron microscopy. An in vitro lipopolysaccharide-treated cell model for bovine endometritis was established to evaluate the correlation between exosome-derived miR-218 and the immune responses. We demonstrated that exosomes could be used to deliver miR-218 from endometrial epithelial cells (EECs) into the uterine microenvironment and adjacent recipient cells to modulate local immune responses. MiR-218 packaged in the exosomes secreted from EECs acts as an inhibitor by blocking immune factors such as interleukin (IL)-6, IL-1b, tumour necrosis factor-a, the chemokines macrophage inflammatory genes We demonstrated that exosomes could be used to deliver miR-218 from endometrial epithelial cells (EECs) into the uterine microenvironment and adjacent recipient cells to modulate local immune responses. miR-218 packaged in the exosomes secreted from EECs acts as an inhibitor by blocking immune factors such as interleukin (IL)-6, IL-1b, tumour necrosis factor-a, the chemokines macrophage inflammatory genes
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