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铜绿假单胞菌的粘附素-鞭毛系统对粘蛋白的识别。

Recognition of mucin by the adhesin-flagellar system of Pseudomonas aeruginosa.

作者信息

Ramphal R, Arora S K, Ritchings B W

机构信息

Department of Medicine, University of Florida, Gainesville 32610, USA.

出版信息

Am J Respir Crit Care Med. 1996 Oct;154(4 Pt 2):S170-4. doi: 10.1164/ajrccm/154.4_Pt_2.S170.

DOI:10.1164/ajrccm/154.4_Pt_2.S170
PMID:8876537
Abstract

Pseudomonas aeruginosa colonizes the mucus of patients with chronic lung diseases by a specific mechanism involving an adhesin-receptor system. Several adhesins have been implicated in the adhesion of P. aeruginosa to cells, but the identity of the principal adhesin(s) involved in adhesion to mucin is unknown. Mutagenesis studies have indicated that P. aeruginosa adhesion is under the control of the rpoN gene, which also regulates pilin synthesis, flagellum formation, and other functions. Mutagenesis of certain flagellar genes that are not controlled by RpoN, e.g., flif, also indicates a close relationship between adhesion and flagellar genes and not necessarily an independent effect of rpoN on adhesion. Mutants of certain early flagellar genes lead to the loss of both adhesion and motility, whereas mutants of certain late genes, e.g., fliC, the gene for flagellin, lose motility but retain adhesion. Recent studies indicate that both motility and adhesion are regulated by a two-component regulatory system called fleS-R, which in turn is controlled by another regulator in a cascade that involves rpoN. A fleR mutant possessing pili adheres poorly to mucins, definitively showing that pili do not play a major role in adhesion to mucin. It is unclear whether the adhesin is a flagellar protein or another protein that uses the flagellar export apparatus for localization or both. Finding the gene under control of rpoN may provide answers to these questions.

摘要

铜绿假单胞菌通过一种涉及粘附素-受体系统的特定机制定殖于慢性肺部疾病患者的黏液中。几种粘附素与铜绿假单胞菌对细胞的粘附有关,但参与与黏蛋白粘附的主要粘附素的身份尚不清楚。诱变研究表明,铜绿假单胞菌的粘附受rpoN基因控制,该基因还调节菌毛素合成、鞭毛形成和其他功能。某些不受RpoN控制的鞭毛基因(如flif)的诱变也表明粘附与鞭毛基因之间存在密切关系,而不一定是rpoN对粘附的独立作用。某些早期鞭毛基因的突变体导致粘附和运动能力丧失,而某些晚期基因(如鞭毛蛋白基因fliC)的突变体失去运动能力但保留粘附能力。最近的研究表明,运动能力和粘附都受一种称为fleS-R的双组分调节系统调控,而该系统又由涉及rpoN的级联中的另一种调节因子控制。具有菌毛的fleR突变体对黏蛋白的粘附性很差,这明确表明菌毛在与黏蛋白的粘附中不起主要作用。尚不清楚粘附素是鞭毛蛋白还是另一种利用鞭毛输出装置进行定位的蛋白,或者两者皆是。找到受rpoN控制的基因可能会为这些问题提供答案。

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