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首页> 外文期刊>Infection and immunity >The Capsule Supports Survival but Not Traversal ofEscherichia coli K1 across the Blood-Brain Barrier
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The Capsule Supports Survival but Not Traversal ofEscherichia coli K1 across the Blood-Brain Barrier

机译：该胶囊支持跨血脑屏障的大肠杆菌K1存活，但不能穿越

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The vast majority of cases of gram-negative meningitis in neonates are caused by K1-encapsulated Escherichia coli. The role of the K1 capsule in the pathogenesis of E. coli meningitis was examined with an in vivo model of experimental hematogenousE. coli K1 meningitis and an in vitro model of the blood-brain barrier. Bacteremia was induced in neonatal rats with theE. coli K1 strain C5 (O18:K1) or its K1?derivative, C5ME. Subsequently, blood and cerebrospinal fluid (CSF) were obtained for culture. Viable bacteria were recovered from the CSF of animals infected with E. coli K1 strains only; none of the animals infected with K1? strains had positive CSF cultures. However, despite the fact that their cultures were sterile, the presence of O18 E. coli was demonstrated immunocytochemically in the brains of animals infected with K1? strains and was seen by staining of CSF samples. In vitro, brain microvascular endothelial cells (BMEC) were incubated with K1+ and K1? E. coli strains. The recovery of viable intracellular organisms of the K1+strain was significantly higher than that for the K1?strain (P = 0.0005). The recovery of viable intracellular K1? E. coli bacteria was increased by cycloheximide treatment of BMEC (P = 0.0059) but was not affected by nitric oxide synthase inhibitors or oxygen radical scavengers. We conclude that the K1 capsule is not necessary for the invasion of bacteria into brain endothelial cells but is responsible for helping to maintain bacterial viability during invasion of the blood-brain barrier.
机译：新生儿中绝大多数革兰氏阴性脑膜炎病例是由包裹K1的大肠杆菌引起的。 K1胶囊在 E发病机理中的作用。用实验性血源性 E的体内模型检查了大肠埃希氏菌脑膜炎。大肠杆菌K1脑膜炎和血脑屏障的体外模型。用emE在新生大鼠中诱发细菌血症。大肠杆菌K1株C5（O18：K1）或其K1 ？衍生物C5ME。随后，获得血液和脑脊液（CSF）进行培养。从感染了 E的动物的脑脊液中回收活细菌。仅是大肠杆菌 K1菌株;感染K1 ？株的动物均无CSF培养阳性。然而，尽管事实上它们的培养物是无菌的，但还是存在O18E。在感染K1 ？菌株的动物的脑中已通过免疫细胞化学方法证实了大肠杆菌。在体外，将脑微血管内皮细胞（BMEC）与K1 + 和K1 ？ E孵育。大肠杆菌菌株。 K1 + 菌株的活细胞内生物的回收率显着高于K1 ？菌株的活度（ P = 0.0005）。活细胞内K1 ？ E的恢复。环己酰亚胺处理BMEC会增加大肠杆菌（ P = 0.0059），但不受一氧化氮合酶抑制剂或氧自由基清除剂的影响。我们得出的结论是，K1胶囊对于细菌侵入脑内皮细胞不是必需的，但可在维持血脑屏障的过程中帮助维持细菌的活力。

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