

畜牧兽医学报 ›› 2025, Vol. 56 ›› Issue (10): 4863-4876.doi: 10.11843/j.issn.0366-6964.2025.10.009
收稿日期:2025-01-10
出版日期:2025-10-23
发布日期:2025-11-01
通讯作者:
李朋,丁家波
E-mail:17861509833@163.com;lipeng01@caas.cn;dingjiabo@caas.cn
作者简介:王恒泰(1998-), 男, 山东滕州人, 博士生, 主要从事布鲁氏菌逃逸宿主先天免疫的分子机制研究。E-mail: 17861509833@163.com
基金资助:
WANG Hengtai(
), JIANG Hui, LI Peng*(
), DING Jiabo*(
)
Received:2025-01-10
Online:2025-10-23
Published:2025-11-01
Contact:
LI Peng, DING Jiabo
E-mail:17861509833@163.com;lipeng01@caas.cn;dingjiabo@caas.cn
摘要:
布鲁氏菌病(brucellosis)是由布鲁氏菌(Brucella spp.)侵染引起的一种人畜共患细菌病, 严重危害人类健康和养殖业发展。布鲁氏菌是一种胞内寄生菌, 逃避宿主天然免疫反应实现胞内寄生是布鲁氏菌毒力的重要体现。脂多糖(LPS)是布鲁氏菌编码的重要毒力因子之一。相较于其他革兰阴性菌, 布鲁氏菌LPS的主要成分、空间结构、连接方式均有不同, 使其表现出特有的低内毒素性, 并且在协助布鲁氏菌逃逸宿主天然免疫系统的识别以及调控免疫应答过程中起关键作用。本文聚焦布鲁氏菌LPS, 对其特殊结构、生物合成过程及其免疫逃逸机制进行综述, 为全面了解布鲁氏菌LPS的生物学功能奠定基础。
中图分类号:
王恒泰, 蒋卉, 李朋, 丁家波. 布鲁氏菌脂多糖的生物合成及其在免疫逃逸中的生物学功能[J]. 畜牧兽医学报, 2025, 56(10): 4863-4876.
WANG Hengtai, JIANG Hui, LI Peng, DING Jiabo. Biosynthesis of Brucella Lipopolysaccharides and Their Biological Functions in Immune Evasion[J]. Acta Veterinaria et Zootechnica Sinica, 2025, 56(10): 4863-4876.
图 2
LPS在S型布鲁氏菌免疫逃逸过程中的作用机制示意图 ①S型布鲁氏菌LPS脂质A的长酰基链抑制宿主TLR4/MD-2的识别和结合;②S型布鲁氏菌LPS的核心寡糖低水平的磷酸化和糖基修饰抑制了补体C1q的结合;③S型布鲁氏菌LPS的O抗原可与宿主细胞膜上的清道夫受体SR-A结合,避免早期与溶酶体融合,保证布鲁氏菌在细胞内的早期存活;④O抗原可通过空间位阻干扰MHC-Ⅱ的递呈过程,降低了抗原呈递的效率;⑤O抗原限制NF-κB信号通路激活,有利于布鲁氏菌在细胞内的存活;⑥O抗原抑制C3转化酶的形成,减少炎性细胞因子的产生、降低补体介导的溶菌作用,有利于布鲁氏菌在细胞内的存活;⑦O抗原抑制ER-Stress信号通路,有利于布鲁氏菌在细胞内的存活;⑧O抗原可以激活巨噬细胞中的PI3K/Akt信号通路,促进被感染的细胞存活,进而有利于布鲁氏菌在细胞内的存活。其中,C3a + C5a是指补体C3片段a和C5片段a是在补体系统激活过程中产生的活性肽;PI3K/Akt是指磷脂酰肌醇-3激酶(PI3K)和蛋白激酶B(Akt)构成的一个重要的信号通路,调控细胞的生长、代谢和存活等多个生理过程;ER-Stress是指内质网应激,内质网功能受到干扰或损害的状态,作为应对机制,细胞启动一系列适应性机制来恢复内质网的稳态,确保蛋白质正确折叠和细胞功能的正常进行;NF-κB是指一类转录因子,广泛参与细胞的免疫反应、炎症反应、细胞增殖、存活和应激反应等多种生理过程"
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