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Listeria monocytogenes Virulence Factors That Stimulate Endothelial Cells

机译：刺激内皮细胞的单核细胞增生李斯特菌毒力因子

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Listeria monocytogenes infection of endothelial cells upregulates surface expression of adhesion molecules and stimulates neutrophil adhesion to infected cell monolayers. The experiments presented here tested the roles of specific bacterial virulence factors as triggers for this inflammatory phenotype and function. Human umbilical vein endothelial cell (HUVEC) monolayers were infected with wild-type L. monocytogenes or L. monocytogenesmutants; then surface expression of E-selectin and neutrophil adhesion were measured. The results showed that Δhly andprfA mutants were the most crippled, requiring 100-fold more mutant bacteria than wild-type bacteria for analogous stimulation. By comparison, L. monocytogenes mutants with deletions ofactA, inlA, inlB,inlAB, plcA, and plcB resembled their parent strains, and a ΔplcA ΔplcB mutant displayed decreased intracellular growth rate but only a minor decrease in stimulation of E-selectin or neutrophil adhesion. Other experiments showed that cytochalasin D-treated HUVEC monolayers bound bacteria, but internalization and increased surface E-selectin and intercellular adhesion molecule-1 expression were profoundly inhibited. However, cytochalasin D had no effect on the HUVEC response to stimulation with lipopolysaccharide or tumor necrosis factor alpha. These data suggest that listeriolysin O production by infecting L. monocytogenes contributes to increased expression of surface E-selectin and intercellular adhesion molecule-1, but neither it nor intracellular replication are directly responsible for this event. Nonetheless it is possible that listeriolysin O potentiates the effect(s) of an other molecule(s) that directly triggers this response. Additionally, cellular invasion by L. monocytogenes appears to be critical for initiating the HUVEC response, potentially by providing a signal which results in upregulation of the necessary bacterial genes.
机译：单核细胞增生李斯特菌感染内皮细胞会上调粘附分子的表面表达，并刺激嗜中性粒细胞粘附到感染的细胞单层。这里介绍的实验测试了特定细菌毒力因子作为这种炎症表型和功能的触发因素的作用。人脐静脉内皮细胞（HUVEC）单层感染了野生型 L。单核细胞增生或 L。单核细胞增生突变体;然后测量E-选择蛋白的表面表达和中性粒细胞粘附。结果表明，Δ hly 和 prfA 突变体最残缺，类似刺激所需的突变菌比野生型菌多100倍。相比之下， L。 actA ， inlA ， inlB ， inlAB ， plcA < / em>和 plcB 与它们的亲本菌株相似，并且Δ plcAΔplcB突变体显示细胞内生长速率降低，但对E-选择素或嗜中性白细胞粘附的刺激仅轻微降低。其他实验表明，细胞松弛素D处理的HUVEC单层结合细菌，但是内化作用和表面E-选择素的增加以及细胞间粘附分子1的表达受到了显着抑制。但是，细胞松弛素D对HUVEC对脂多糖或肿瘤坏死因子α刺激的反应没有影响。这些数据表明通过感染 L可以产生李斯特菌溶血素O。单核细胞增生因子有助于增加表面E-选择蛋白和细胞间粘附分子1的表达，但它和细胞内复制均不是造成此事件的直接原因。然而，李斯特菌溶血素O可能会增强直接触发该反应的其他分子的作用。此外， L对细胞的侵袭。单核细胞增生对于启动HUVEC应答至关重要，可能是通过提供信号导致必需细菌基因上调的信号。

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