首页|鼠疫耶尔森菌LPS结构变异机制及其免疫逃逸功能研究进展

鼠疫耶尔森菌LPS结构变异机制及其免疫逃逸功能研究进展

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鼠疫是鼠疫耶尔森菌(以下简称鼠疫菌)引起的一种自然疫源性传染病.鼠疫菌不仅能编码多种毒力因子破坏宿主免疫信号传导,还能修饰其脂多糖的结构,逃逸宿主免疫监视并强烈抑制宿主的免疫响应,是其高致病性形成的重要分子机制之一.鼠疫菌LPS缺乏O抗原,脂质A结构也具有特殊的温度转换调控机制,在不同温度下可形成具有不同数目酰基侧链的脂质A,在其逃逸宿主固有免疫识别和清除中发挥重要作用.本文将对鼠疫菌脂多糖(lipopolysaccharide,LPS)的生物合成调控、结构变异及其免疫逃逸机制的研究进展做一综述,为研究病原菌利用LPS结构修饰逃避宿主固有免疫防御的分子机制提供借鉴.
Advances in lipopolysaccharide structural variations and immune escape in Yersinia pestis
Plague,caused by Yersinia pestis,is a zoonotic disease that infects both humans and animals.Y.pestis not only encodes various virulence factors that can disrupt host immune signaling but also can modify its lipopolysaccharide(LPS)struc-ture,thereby evading host immune surveillance and potently suppressing the host's immune response,in an important molecu-lar mechanism underlying its high pathogenicity.The LPS of Y.pestis lacks an O antigen,and its lipid A structure possesses a unique temperature transition regulatory mechanism.At different temperatures,Y.pestis forms lipid A with different numbers of acyl side chains,which plays a pivotal role in the evasion of host innate immune recognition and clearance.Here,we present a comprehensive review of research progress in the biosynthetic regulation,structural variation,and immune escape mechanism of Y.pestis LPS,to provide a reference for the study of the molecular mechanisms of pathogens using LPS structural modifica-tions to elude host innate immune defenses.

Yersinia pestislipopolysaccharide(LPS)immune escape

冯文静、张源、杜宗敏

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牡丹江医学院公共卫生学院,牡丹江 157011

军事科学院军事医学研究院微生物流行病研究所,病原微生物生物安全全国重点实验室,北京 100071

鼠疫菌 脂多糖 免疫逃逸

病原微生物生物安全全国重点实验室自主课题

SKLPBS2211

2024

中国人兽共患病学报
中国微生物学会

中国人兽共患病学报

CSTPCD北大核心
影响因子:0.814
ISSN:1002-2694
年,卷(期):2024.40(9)
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