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首页> 外文期刊>Infection and immunity >NlpI Contributes to Escherichia coli K1 Strain RS218 Interaction with Human Brain Microvascular Endothelial Cells
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NlpI Contributes to Escherichia coli K1 Strain RS218 Interaction with Human Brain Microvascular Endothelial Cells

机译：NlpI有助于大肠杆菌K1株RS218与人脑微血管内皮细胞的相互作用

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摘要

Escherichia coli K1 is the most common Gram-negative bacillary organism causing neonatal meningitis. E. coli K1 binding to and invasion of human brain microvascular endothelial cells (HBMECs) is a prerequisite for its traversal of the blood-brain barrier (BBB) and penetration into the brain. In the present study, we identified NlpI as a novel bacterial determinant contributing to E. coli K1 interaction with HBMECs. The deletion of nlpI did not affect the expression of the known bacterial determinants involved in E. coli K1-HBMEC interaction, such as type 1 fimbriae, flagella, and OmpA, and the contribution of NlpI to HBMECs binding and invasion was independent of those bacterial determinants. Previous reports have shown that the nlpI mutant of E. coli K-12 exhibits growth defect at 42°C at low osmolarity, and its thermosensitive phenotype can be suppressed by a mutation on the spr gene. The nlpI mutant of strain RS218 exhibited similar thermosensitive phenotype, but additional spr mutation did not restore the ability of the nlpI mutant to interact with HBMECs. These findings suggest the decreased ability of the nlpI mutant to interact with HBMECs is not associated with the thermosensitive phenotype. NlpI was determined as an outer membrane-anchored protein in E. coli, and the nlpI mutant was defective in cytosolic phospholipase A2α (cPLA2α) phosphorylation compared to the parent strain. These findings illustrate the first demonstration of NlpI's contribution to E. coli K1 binding to and invasion of HBMECs, and its contribution is likely to involve cPLA2α.
机译：大肠杆菌K1是引起新生儿脑膜炎的最常见的革兰氏阴性细菌。大肠杆菌K1与人脑微血管内皮细胞（HBMEC）的结合和入侵是其穿越血脑屏障（BBB）并渗透到脑中的先决条件。在本研究中，我们确定了NlpI是一种新的细菌决定簇，有助于大肠杆菌K1与HBMEC相互作用。 nlpI的删除不影响参与大肠杆菌K1-HBMEC相互作用的已知细菌决定簇的表达，例如1型菌毛，鞭毛和OmpA，并且NlpI对HBMEC结合和入侵的贡献独立于那些细菌行列式。以前的报道表明，大肠杆菌K-12的nlpI突变体在低渗透压下于42°C表现出生长缺陷，并且其热敏表型可以通过spr基因上的突变来抑制。 RS218菌株的nlpI突变体表现出相似的热敏表型，但其他spr突变并未恢复nlpI突变体与HBMEC相互作用的能力。这些发现表明，nlpI突变体与HBMEC相互作用的能力降低与热敏表型无关。 NlpI被确定为大肠杆菌中的外膜锚定蛋白，与亲本菌株相比，nlpI突变体在胞质磷脂酶A2α（cPLA2α）磷酸化方面存在缺陷。这些发现说明了NlpI对大肠杆菌K1与HBMEC结合和入侵的贡献的首次证明，其贡献可能涉及cPLA2α。

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