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支原体的遗传变异及其对发病机制的影响。

Mycoplasma genetic variation and its implication for pathogenesis.

作者信息

Citti C, Rosengarten R

机构信息

Institute of Bacteriology and Animal Hygiene, University of Veterinary Medicine, Vienna, Austria.

出版信息

Wien Klin Wochenschr. 1997 Aug 8;109(14-15):562-8.

PMID:9286060
Abstract

Several pathogenic mycoplasma species are known etiologic agents of diseases in man and animals, which typically involve the respiratory tract, urogenital tract and joints and often show chronicity. Although the basis for this chronicity is not well understood, it is apparent that several species of pathogenic mycoplasmas are endowed with a sophisticated genetic machinery for altering their surface attributes. This surface phenotypic variation is thought to play a key role in the establishment and persistence of mycoplasma infections by enabling evasion of host defences and by ensuring adaptation to the rapidly changing microenvironmental conditions encountered in the host. The variability of mycoplasma surface characteristics results both from reversible ON- and OFF-switching of distinct membrane surface proteins (phase variation), from structural changes of these proteins (size variation) and from changes in their surface presentation (epitope masking and demasking). The majority of these surface proteins that are subject to variation are encoded by multiple variant single-copy genes and are lipid-modified proteins which represent the major coat proteins and surface antigens of several pathogenic mycoplasmas. Variable surface lipoproteins play an important role in the pathogenesis of a mycoplasma infection by providing escape from immune response, and probably by influencing both colonization of and translocation across the mucosal barrier. In this minireview, recent developments regarding the genetic mechanisms and the functional significance of surface lipoprotein variation in the pathogenesis of mycoplasma infections are summarized.

摘要

几种致病性支原体是人和动物疾病的已知病原体,通常累及呼吸道、泌尿生殖道和关节,且常呈慢性病程。尽管这种慢性病程的基础尚不清楚,但显然几种致病性支原体具有复杂的遗传机制来改变其表面特性。这种表面表型变异被认为在支原体感染的建立和持续存在中起关键作用,它能够逃避宿主防御,并确保适应宿主中快速变化的微环境条件。支原体表面特征的变异性既源于不同膜表面蛋白的可逆开启和关闭切换(相变)、这些蛋白结构的变化(大小变异),也源于其表面呈现的变化(表位掩盖和去掩盖)。这些易发生变异的表面蛋白大多数由多个可变单拷贝基因编码,并且是脂质修饰蛋白,它们是几种致病性支原体的主要外膜蛋白和表面抗原。可变表面脂蛋白通过逃避免疫反应,可能还通过影响在粘膜屏障上的定植和转运,在支原体感染的发病机制中起重要作用。在这篇综述中,总结了关于支原体感染发病机制中表面脂蛋白变异的遗传机制和功能意义的最新进展。

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