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首页> 外文期刊>Infection and immunity >Outer Membrane Protein A-Promoted Actin Condensation of Brain Microvascular Endothelial Cells Is Required for Escherichia coli Invasion
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Outer Membrane Protein A-Promoted Actin Condensation of Brain Microvascular Endothelial Cells Is Required for Escherichia coli Invasion

机译：大肠杆菌入侵需要脑微血管内皮细胞的外膜蛋白A促进的肌动蛋白凝集。

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Escherichia coli is the most common gram-negative bacterium that causes meningitis during the neonatal period. We have previously shown that the entry of circulating E. coliorganisms into the central nervous system is due to their ability to invade the blood-brain barrier, which is composed of a layer of brain microvascular endothelial cells (BMEC). In this report, we show by transmission electron microscopy that E. coli transmigrates through BMEC in an enclosed vacuole without intracellular multiplication. The microfilament-disrupting agents cytochalasin D and latrunculin A completely blocked E. coli invasion of BMEC. Cells treated with the microtubule inhibitors nocodazole, colchicine, vincristin, and vinblastine and the microtubule-stabilizing agent taxol also exhibited 50 to 60% inhibition of E. coli invasion. Confocal laser scanning fluorescence microscopy showed F-actin condensation associated with the invasive E. coli but no alterations in microtubule distribution. These results suggest thatE. coli uses a microfilament-dependent phagocytosis-like endocytic mechanism for invasion of BMEC. Previously we showed that OmpA expression significantly enhances the E. coliinvasion of BMEC. We therefore examined whether OmpA expression is related to the recruitment of F-actin. OmpA+ E. coli induced the accumulation of actin in BMEC to a level similar to that induced by the parental strain, whereas OmpA? E. coli did not. Despite the presence of OmpA, a noninvasive E. coli isolate, however, did not show F-actin condensation. OmpA+-E. coli-associated condensation of F-actin was blocked by synthetic peptides corresponding to the N-terminal extracellular domains of OmpA as well as BMEC receptor analogues for OmpA, chitooligomers (GlcNAcβ1-4GlcNAc oligomers). These findings suggest that OmpA interaction is critical for the expression or modulation of other bacterial proteins that will subsequently cause actin accumulation for the uptake of bacteria.
机译：大肠杆菌是最常见的革兰氏阴性细菌，可在新生儿期引起脑膜炎。先前我们已经显示了循环 E的条目。大肠杆菌进入中枢神经系统的原因是它们能够入侵血脑屏障，后者由一层脑微血管内皮细胞（BMEC）组成。在本报告中，我们通过透射电子显微镜显示了 E。 通过封闭的液泡中的BMEC迁移，而没有细胞内增殖。微丝破坏剂细胞松弛素D和拉特朗库菌素A完全阻断了 E。大肠杆菌对BMEC的入侵。用微管抑制剂诺考达唑，秋水仙碱，长春新碱和长春花碱以及微管稳定剂紫杉醇处理的细胞也表现出50-60％的Em抑制作用。大肠杆菌入侵。共聚焦激光扫描荧光显微术显示F-肌动蛋白凝集与侵袭性 E有关。大肠杆菌，但微管分布没有改变。这些结果表明 E。 利用微丝依赖性的吞噬作用样内吞机制入侵BMEC。先前我们显示OmpA表达可显着增强 E。大肠杆菌对BMEC的入侵。因此，我们检查了OmpA表达是否与F-肌动蛋白的募集有关。 OmpA + E。大肠杆菌诱导肌动蛋白在BMEC中的积累达到与亲本菌株诱导的肌动蛋白相似的水平，而OmpA ？ E。大肠没有。尽管存在OmpA，但它是非侵入性的 E。但是，大肠杆菌分离物未显示F-肌动蛋白凝集。 OmpA + - E。 F-肌动蛋白的大肠埃希菌相关缩合被对应于OmpA N末端胞外域的合成肽以及OmpA的BMEC受体类似物，壳寡聚体（GlcNAcβ1-4GlcNAc寡聚体）阻断。这些发现表明，OmpA相互作用对于其他细菌蛋白的表达或调节至关重要，这些蛋白随后会引起肌动蛋白的积累，从而吸收细菌。

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