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首页> 外文期刊>Infection and immunity >NlpI Facilitates Deposition of C4bp on Escherichia coli by Blocking Classical Complement-Mediated Killing, Which Results in High-Level Bacteremia
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NlpI Facilitates Deposition of C4bp on Escherichia coli by Blocking Classical Complement-Mediated Killing, Which Results in High-Level Bacteremia

机译：NlpI通过阻止经典补体介导的杀伤作用促进大肠杆菌上C4bp的沉积，导致高水平细菌血症

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摘要

Neonatal meningitis Escherichia coli (NMEC) is the most common Gram-negative organism that is associated with neonatal meningitis, which usually develops as a result of hematogenous spread of the bacteria. There are two key pathogenesis processes for NMEC to penetrate into the brain, the essential step for the development of E. coli meningitis: a high-level bacteremia and traversal of the blood-brain barrier (BBB). Our previous study has shown that the bacterial outer membrane protein NlpI contributes to NMEC binding to and invasion of brain microvascular endothelial cells, the major component cells of the BBB, suggesting a role for NlpI in NMEC crossing of the BBB. In this study, we showed that NlpI is involved in inducing a high level of bacteremia. In addition, NlpI contributed to the recruitment of the complement regulator C4bp to the surface of NMEC to evade serum killing, which is mediated by the classical complement pathway. NlpI may be involved in the interaction between C4bp and OmpA, which is an outer membrane protein that directly interacts with C4bp on the bacterial surface. The involvement of NlpI in two key pathogenesis processes of NMEC meningitis may make this bacterial factor a potential target for prevention and therapy of E. coli meningitis.
机译：新生儿脑膜炎大肠埃希菌（NMEC）是与新生儿脑膜炎有关的最常见的革兰氏阴性菌，通常是由于细菌的血源性传播而形成的。 NMEC进入大脑有两个关键的发病机理过程，这是发展大肠杆菌脑膜炎的关键步骤：高水平菌血症和血脑屏障（BBB）的穿越。我们以前的研究表明，细菌外膜蛋白NlpI有助于NMEC与脑微血管内皮细胞（BBB的主要组成细胞）结合和侵袭，提示NlpI在BBB的NMEC穿越中发挥了作用。在这项研究中，我们表明NlpI参与诱导高水平的菌血症。此外，NlpI有助于补体调节剂C4bp募集到NMEC表面，以逃避血清杀伤，这是由经典补体途径介导的。 NlpI可能参与C4bp和OmpA之间的相互作用，OmpA是一种直接与细菌表面C4bp相互作用的外膜蛋白。 NlpI参与NMEC脑膜炎的两个关键发病机制可能使该细菌因子成为预防和治疗大肠杆菌脑膜炎的潜在靶标。

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