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首页> 外文期刊>Infection and immunity >Bartonella henselae Induces NF-κB-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors
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Bartonella henselae Induces NF-κB-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors

机译：汉赛巴尔通体在培养的人内皮细胞中诱导粘附分子的NF-κB依赖性上调：外膜蛋白作为致病因素的可能作用

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The endothelium is a specific target for Bartonella henselae, and endothelial cell infection represents an important step in the pathogenesis of cat scratch disease and bacillary angiomatosis. Mechanisms of Bartonella-endothelial cell interaction as well as signaling pathways involved in target cell activation were analyzed. B. henselae strain Berlin-1, isolated from bacillary angiomatosis lesions of a human immunodeficiency virus-infected patient, potently stimulated human umbilical cord vein endothelial cells (HUVEC), as determined by NF-κB activation and enhanced adhesion molecule expression. These effects were accompanied by increased PMN rolling on and adhesion to infected endothelial cell monolayers, as measured in a parallel-plate flow chamber assay. Monoclonal antibodies against E-selectin significantly reduced PMN rolling and adhesion. In our hands, B. henselae Berlin-1 was substantially more active than the typing strain B. henselae ATCC 49882. E-selectin and ICAM-1 upregulation occurred for up to 9 days, as verified by Northern blotting and cell surface enzyme-linked immunosorbent assay. Induction of adhesion molecules was mediated via NF-κB activation and could be blocked by a specific NF-κB inhibitor. Additional studies indicated that B. henselae-induced effects did not require living bacteria or Bartonella lipopolysaccharides. Exposure of HUVEC to purified B. henselae outer membrane proteins (OMPs), however, reproduced all aspects of endothelial cell activation. In conclusion, B. henselae, the causative agent of cat scratch disease and bacillary angiomatosis, infects and activates endothelial cells. B. henselae OMPs are sufficient to induce NF-κB activation and adhesion molecule expression followed by enhanced rolling and adhesion of leukocytes. These observations identify important new properties of B. henselae, demonstrating its capacity to initiate a cascade of events culminating in a proinflammatory phenotype of infected endothelial cells.
机译：内皮是 Bartonella henselae 的特定靶标，内皮细胞感染是猫抓痕病和细菌性血管瘤病发病机理中的重要一步。分析了 Bartonella -内皮细胞相互作用的机制以及与靶细胞活化有关的信号通路。 B。从人类免疫缺陷病毒感染患者的细菌性血管瘤病病变中分离出的亨塞莱氏菌柏林-1株，通过NF-κB活化和增强的黏附分子表达确定，可有效刺激人脐带静脉内皮细胞（HUVEC）。这些作用伴随着PMN滚动的增加以及对感染的内皮细胞单层的粘附，如在平行板流动室测定中所测量的。针对E-选择素的单克隆抗体可显着降低PMN滚动和粘附。在我们手中， B。 henselae Berlin-1的活性明显强于打字株 B。 henselae ATCC49882。Northern印迹和细胞表面酶联免疫吸附试验证实，E-选择素和ICAM-1上调的过程长达9天。粘附分子的诱导是通过NF-κB激活介导的，并且可以被特定的NF-κB抑制剂阻断。进一步的研究表明， B。 henselae 诱导的作用不需要活细菌或 Bartonella 脂多糖。 HUVEC暴露于纯化的 B。 henselae 外膜蛋白（OMPs）复制了内皮细胞激活的所有方面。总之， B。猫抓痒病和细菌性血管瘤病的病原体henselae 感染并激活内皮细胞。 B。 henselae OMPs足以诱导NF-κB活化和粘附分子表达，然后增强白细胞的滚动和粘附。这些观察结果确定了 B的重要新特性。 henselae ，证明了其启动一系列事件的能力，这些事件最终导致被感染的内皮细胞的促炎表型。

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