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肺炎支原体细胞黏附:解开连接的纽带

Mycoplasma pneumoniae cytadherence: unravelling the tie that binds.

作者信息

Krause D C

机构信息

Department of Microbiology, University of Georgia, Athens 30602, USA.

出版信息

Mol Microbiol. 1996 Apr;20(2):247-53. doi: 10.1111/j.1365-2958.1996.tb02613.x.

Abstract

Mycoplasma pneumoniae is the leading cause of pneumonia in older children and young adults. Mycoplasma adherence to the respiratory epithelium (cytadherence) is required for colonization and pathogenesis. Although considered to be among the smallest and simplest known prokaryotes, this cell-wall-less bacterium possesses a highly differentiated terminal structure that is thought to be functional in mycoplasma cell division, gliding motility, and cytadherence. Mutant analysis has identified mycoplasma proteins associated with cytadherence, and revealed novel regulatory features. Ultrastructural and biochemical studies have established the subcellular location and interaction of key components, several of which are phosphorylated by ATP-dependent kinase(s) in a manner that is responsive to changing nutritional conditions. This review summarizes recent progress in defining the composition, organization and regulation of the attachment organelle. What emerges is a picture of M. pneumoniae cytadherence as a multifactorial process that extends well beyond adhesin-receptor recognition.

摘要

肺炎支原体是大龄儿童和青年成人肺炎的主要病因。肺炎支原体在呼吸道上皮的黏附(细胞黏附)是其定植和发病机制所必需的。尽管被认为是已知最小且最简单的原核生物之一,但这种无细胞壁的细菌拥有高度分化的末端结构,该结构被认为在支原体细胞分裂、滑行运动和细胞黏附中发挥作用。突变分析已鉴定出与细胞黏附相关的支原体蛋白,并揭示了新的调控特征。超微结构和生化研究确定了关键成分的亚细胞定位和相互作用,其中几种成分会被依赖ATP的激酶磷酸化,其方式对不断变化的营养条件有反应。本综述总结了在确定附着细胞器的组成、组织和调控方面的最新进展。由此呈现出的肺炎支原体细胞黏附图景是一个多因素过程,远远超出了黏附素-受体识别的范畴。

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