OmpR-dependent and OmpR-independent responses of Escherichia coli to sublethal attack by the neutrophil bactericidal/permeability increasing protein.
OmpR-dependent and OmpR-independent responses of Escherichia coli to sublethal attack by the neutrophil bactericidal/permeability increasing protein.
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大肠杆菌对中性粒细胞杀菌/通透性增加蛋白的亚致死攻击的 OmpR 依赖性和 OmpR 独立反应。
DOI：
10.1046/j.1365-2958.2002.02804.x
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发表时间：
2002
影响因子：
3.6
通讯作者：
Weiss,Jerrold
中科院分区：
文献类型：
--
作者：
Prohinar,Polonca;Forst,SteveA;Reed,Deoine;Mandic-Mulec,Ines;Weiss,Jerrold
中性粒细胞的杀菌/通透性增加蛋白（BPI）是一种脂多糖（LPS）结合抗菌蛋白，对革兰氏阴性菌具有特异性。 BPI 与细菌表面的结合迅速引发潜在可逆的细菌生长抑制和外膜改变，随后导致内膜破坏和致命损伤。最初的影响包括外膜孔蛋白（OmpF 和 OmpC）合成中选择性 OmpR 依赖性变化。由于 OmpR 是一种全局转录调节因子，我们研究了它在大肠杆菌反应中的可能作用。 BPI引起的大肠杆菌亚致死损伤。 BPI 对细菌菌落形成能力和外膜通透性的早期（<15 分钟）可逆影响在同基因野生型 (wt) andompR−E 中几乎相同。两种菌株均可在 Mg2+ 诱导结合 BPI 位移后修复外膜渗透屏障。然而，OmpR 对于 E 的能力至关重要。 colito 可耐受低剂量的 BPI，并避免亚致死至致死损伤的进展。扫描电子显微镜显示，BPI 处理在 theompR− 菌株中产生了更大的膜扰动，甚至在致死损伤之前就很明显。这些发现表明E的命运。暴露于 BPI 的大肠杆菌依赖于参与外膜修复的 OmpR 独立机制和调节孔蛋白合成并延缓损伤从外膜到内膜进展的 OmpR 依赖过程。
Bactericidal/permeability‐increasing protein (BPI) of neutrophils is a lipopolysaccharide (LPS)‐binding antibacterial protein with specificity for Gramnegative bacteria. BPI binding to the bacterial surface rapidly triggers potentially reversible bacterial growth inhibition and alterations of the outer membrane and, later, disruption of the inner membrane and lethal injury. Initial effects include selective OmpR‐dependent changes in the synthesis of outer membrane porins (OmpF and OmpC). Because OmpR is a global transcriptional regulator, we have examined its possible role in responses ofE. colito sublethal injury caused by BPI. Early (<15 min) reversible effects of BPI on bacterial colony‐forming ability and outer membrane permeability were virtually identical in isogenic wild‐type (wt) andompR−E. coli.Both strains could repair the outer membrane permeability barrier after Mg2+‐induced displacement of bound BPI. However, OmpR was essential for the ability ofE. colito tolerate low doses of BPI and escape the progression of sublethal to lethal damage. Scanning electron microscopy revealed that BPI treatment produced greater membrane perturbations in theompR−strain, apparent even before lethal injury. These findings suggest that the fate ofE. coliexposed to BPI depends on both OmpR‐independent mechanisms engaged in outer membrane repair and OmpR‐ dependent processes that modulate porin synthesis and retard progression of injury from the outer to the inner membrane.