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S2 脂多糖损害了小鼠早孕时的蜕膜化进程。

Lipopolysaccharides of S2 Impaired the Process of Decidualization in Early Pregnancy in Mice.

机构信息

Key Laboratory of Animal Biotechnology of the Ministry of Agriculture and Rural Affairs, Northwest A&F University, Xianyang 712100, China.

College of Veterinary Medicine, Northwest A&F University, Xianyang 712100, China.

出版信息

Toxins (Basel). 2023 Nov 16;15(11):662. doi: 10.3390/toxins15110662.

DOI:10.3390/toxins15110662
PMID:37999525
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10675612/
Abstract

is a notorious zoonotic disease caused by , which can lead to reproductive diseases in humans and animals, such as infertility and abortion. Lipopolysaccharides (LPS) are the main virulence factor of . LPS derived from are different and non-classical and are less toxic and less active than LPS isolated from However, the effects and possible mechanisms of LPS-caused pregnancy loss remain to be revealed. In the present study, we investigated the effects of S2 LPS on early pregnancy loss in mice. The results indicated that embryo implantation failure was induced by LPS treatment in a dose-dependent manner. The injection of 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 LPS treatment in vitro. In summary, 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.

摘要

是一种臭名昭著的人畜共患病,由 引起,可导致人类和动物的生殖疾病,如不孕和流产。脂多糖(LPS)是 的主要毒力因子。 来源的 LPS 不同且是非经典的,其毒性和活性比从 中分离出的 LPS 低。然而, 引起的妊娠丢失的影响和可能的机制仍有待揭示。在本研究中,我们研究了 S2 LPS 对小鼠早期妊娠丢失的影响。结果表明,LPS 处理以剂量依赖性方式诱导胚胎着床失败。LPS 的注射主要导致在交配后第 6 天(dpc)子宫蜕膜区的纤维蛋白溶解,在第 8 dpc 胚胎附近蜕膜细胞中的大颗粒细胞浸润,蜕膜区大量出现间隙,以及胚胎周围的细胞坏死。此外,第 7 天和第 8 天子宫中 Cyclin D3 mRNA 的表达以及第 6 天和第 7 天子宫中 IGFBP-1 mRNA 和孕激素受体的表达也受到抑制。此外,LPS 处理还抑制了子宫内膜基质细胞中蜕膜化标记物 Cyclin D3 和蜕膜化泌乳素相关蛋白(dPRP)的表达。总之,LPS 通过影响蜕膜结构和子宫内膜基质细胞中蜕膜标记因子的表达来影响小鼠的子宫内膜蜕膜化过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/f9341ea5c027/toxins-15-00662-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/04765800af52/toxins-15-00662-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/c0c388a0282b/toxins-15-00662-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/6014b5344926/toxins-15-00662-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/6fee50da5536/toxins-15-00662-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/f9341ea5c027/toxins-15-00662-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/04765800af52/toxins-15-00662-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/c0c388a0282b/toxins-15-00662-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/6014b5344926/toxins-15-00662-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/6fee50da5536/toxins-15-00662-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f4/10675612/f9341ea5c027/toxins-15-00662-g005.jpg

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