Extended-spectrum β-lactamases and the permeability barrier
Extended-spectrum β-lactamases and the permeability barrier
复制标题
DOI：
10.1111/j.1469-0691.2007.01860.x
复制
发表时间：
2008-01-01
影响因子：
14.2
通讯作者：
Martinez-Martinez, L.
中科院分区：
文献类型：
--
作者：
Martinez-Martinez, L.
革兰氏阴性菌的外膜代表亲水性化合物渗透的屏障。孔蛋白（充满水的蛋白质通道）的丢失有助于抗菌素耐药性，特别是当表达额外的耐药机制时。关于大肠杆菌K-12中孔蛋白的结构和调节的许多研究是可用的，但是关于该物种的临床分离株的信息很少。肺炎克雷伯菌主要产生两种孔蛋白OmpK 35和OmpK 36，但许多产超广谱β-内酰胺酶（ESBL）的肺炎克雷伯菌也存在。肺炎分离株不表达OmpK 35。产ESBL克雷伯氏菌OmpK 35和OmpK 36均缺失。肺炎引起对头孢西丁的耐药性、对广谱头孢菌素的耐药性增加以及对碳青霉烯类（特别是厄他培南）的敏感性降低。孔蛋白损失也降低了产ESBL生物对其他非β-内酰胺化合物（如氟喹诺酮类）的敏感性。
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 P-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-p-lactam compounds, such as fluoroquinolones, of ESBL-producing organisms.