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超广谱β-内酰胺酶与通透性屏障

Extended-spectrum beta-lactamases and the permeability barrier.

作者信息

Martínez-Martínez L

机构信息

Service of Microbiology, University Hospital Marqués de Valdecilla, Santander, Spain.

出版信息

Clin Microbiol Infect. 2008 Jan;14 Suppl 1:82-9. doi: 10.1111/j.1469-0691.2007.01860.x.

Abstract

The outer membrane of Gram-negative bacteria represents a barrier for penetration of hydrophilic compounds. Loss of porins (water-filled protein channels) contributes to antimicrobial resistance, particularly when additional mechanisms of resistance are expressed. Many studies on the structure and regulation of porins in Escherichia coli K-12 are available, but there is little information concerning clinical isolates of this species. In Klebsiella pneumoniae, two major porins, OmpK35 and OmpK36, are produced, but many extended-spectrum beta-lactamase (ESBL)-producing K. pneumoniae isolates do not express OmpK35. Loss of both OmpK35 and OmpK36 in ESBL-producing K. pneumoniae causes resistance to cefoxitin, increased resistance to expanded-spectrum cephalosporins, and decreased susceptibility to carbapenems, particularly ertapenem. Porin loss also decreases the susceptibility to other non-beta-lactam compounds, such as fluoroquinolones, of ESBL-producing organisms.

摘要

革兰氏阴性菌的外膜是亲水性化合物穿透的屏障。孔蛋白(充满水的蛋白质通道)的缺失会导致抗菌药物耐药性,尤其是当表达其他耐药机制时。关于大肠杆菌K-12中孔蛋白的结构和调控已有许多研究,但关于该物种临床分离株的信息很少。肺炎克雷伯菌产生两种主要孔蛋白OmpK35和OmpK36,但许多产超广谱β-内酰胺酶(ESBL)的肺炎克雷伯菌分离株不表达OmpK35。产ESBL的肺炎克雷伯菌中OmpK35和OmpK36均缺失会导致对头孢西丁耐药,对广谱头孢菌素的耐药性增加,对碳青霉烯类药物,尤其是厄他培南的敏感性降低。孔蛋白缺失还会降低产ESBL菌株对其他非β-内酰胺类化合物(如氟喹诺酮类)的敏感性。

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