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脂多糖的生物学功能及其在奶牛子宫内膜炎中的作用机制OA

The Biological Function of Lipopolysaccharide and Its Mechanism in Bovine Endometritis

中文摘要英文摘要

子宫内膜炎是奶牛常见的生殖系统疾病,其发病率长期居高不下,严重制约着奶牛养殖业的经济效益.该病的发生主要与细菌感染有关,其中革兰氏阴性菌是诱发奶牛子宫内膜炎的主要致病菌,可引起奶牛发情周期紊乱、排卵障碍、降低子宫内环境适配性等,最终造成奶牛受孕率下降.革兰氏阴性菌细胞壁中的脂多糖是关键毒力因子,脂多糖通过与奶牛子宫内膜宿主细胞表面的 Toll 样受体 4(Toll-like Receptor 4,TLR4)发生特异性结合,诱导 TLR4 构象改变来激活下游信号传导通路,促使免疫细胞释放大量炎性因子,导致子宫内膜组织发生病理性损伤.鉴于脂多糖在奶牛子宫内膜炎致病机制中的核心地位,明确其生物学功能及与宿主细胞间的互作机制,已成为防治奶牛子宫内膜炎的前提.本文综述了脂多糖的生物学功能,并阐明脂多糖-TLR4信号通路在奶牛子宫内膜炎中的调控机制,旨在为防治奶牛子宫内膜炎提供理论依据和潜在作用靶点.

Dairy bovine endometritis is a common reproductive disorder in postpartum dairy cows.Multiple factors including dystocia,retained placenta,bacterial infection,and improper feeding and management can trigger this disease and further result in reproductive problems such as abnormal estrus and reduced conception rate.Among the various pathogenic factors of endometritis,bacterial infection serves as the primary cause,with Gram-negative bacterial infection being the most prevalent.Lipopolysaccharide,a unique component of the cell wall of Gram-negative bacteria,is one of the key factors contributing to the occurrence of dairy bovine endometritis.In cases of bovine endometritis,lipopolysaccharide initiates a series of signal transduction cascades by specifically binding to Toll-like receptor 4(TLR4)on the surface of host cells,which ultimately induces the activation of immune cells and massive release of cytokines,thereby causing inflammatory damage to the endometrium.This paper therefore reviews the biological functions of lipopolysaccharide and its underlying mechanisms in dairy bovine endometritis,aiming to provide a theoretical reference for exploring efficient prevention and treatment strategies for this disease.

程珍珍;马燕芬;杨文飞;赵洪喜

宁夏大学动物科技学院,宁夏 银川 750021宁夏大学动物科技学院,宁夏 银川 750021宁夏新澳农牧有限公司,宁夏 银川 750406宁夏大学动物科技学院,宁夏 银川 750021

农业科技

脂多糖奶牛子宫内膜炎信号通路炎性因子

LipopolysaccharideBovine endometritisSignal pathwayInflammatory factors

《中国畜牧杂志》 2026 (9)

69-75,84,8

银川市科技计划项目区域协同创新专项(2024QYXT003)宁夏大学产教融合研究生联合培养示范基地建设项目

10.19556/j.0258-7033.20250703-01

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