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

Advances in lipopolysaccharide structural variations and immune escape in Yersinia pestis

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。

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)structure,thereby evading host immune surveillance and potently suppressing the host's immune response,in an important molecular 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 modifications to elude host innate immune defenses.