| Summary: | <i>Brucellosis</i> is a notorious zoonotic disease caused by <i>Brucella</i>, which can lead to reproductive diseases in humans and animals, such as infertility and abortion. Lipopolysaccharides (LPS) are the main virulence factor of <i>Brucella</i>. LPS derived from <i>Brucella</i> are different and non-classical and are less toxic and less active than LPS isolated from <i>E. coli.</i> However, the effects and possible mechanisms of <i>Brucella</i> LPS-caused pregnancy loss remain to be revealed. In the present study, we investigated the effects of <i>Brucella suis</i> S2 LPS on early pregnancy loss in mice. The results indicated that embryo implantation failure was induced by <i>Brucella</i> LPS treatment in a dose-dependent manner. The injection of <i>Brucella</i> LPS mainly resulted in fibrinolysis in the decidual area of the uterus on the 6th day post coition (dpc), infiltration of large granular cells among the decidual cells near the embryo on the 8th dpc, a large number of gaps in the decidual area, and cell necrosis around the embryo. In addition, the expression of Cyclin D3 mRNA in the uterus on the 7th and 8th dpc and IGFBP-1 mRNA and the progesterone receptor in the uterus on the 6th and 7th dpc were also inhibited. Moreover, the expression of decidualization marker Cyclin D3 and decidualization prolactin-associated protein (dPRP) in endometrial stromal cells were also inhibited by <i>Brucella</i> LPS treatment in vitro. In summary, <i>Brucella</i> LPS affect the process of endometrial decidualization in mice by affecting the structure of the decidua and the expression of decidual marker factors in endometrial stromal cells.
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