Helicobacter pylori-induced activation of human endothelial cells
Helicobacter pylori-induced activation of human endothelial cells
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DOI：
10.1128/iai.70.8.4581-4590.2002
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发表时间：
2002-08-01
影响因子：
3.1
通讯作者：
Quiding-Järbrink, M
中科院分区：
文献类型：
--
作者：
Innocenti, M;Thoreson, AC;Quiding-Järbrink, M
幽门螺杆菌感染引起慢性炎症，中性粒细胞持续聚集到发炎的胃粘膜。为了评估内皮细胞在这一过程中的作用，我们检测了粘附分子的表达和趋化因子和细胞因子的产生，从人脐静脉内皮细胞刺激的充分表征H。pylori菌株以及纯化的蛋白质。我们的研究结果表明，内皮细胞积极促进中性粒细胞的募集，因为刺激与H。幽门螺杆菌诱导粘附分子VCAM-1、ICAM-1和E-选择素以及趋化因子白细胞介素8（IL-8）和生长相关癌基因α（GRO-α）和细胞因子IL-6的上调。然而，不同的H. pylori菌株刺激内皮细胞。这些菌株间的变异与菌株是否分离自十二指肠溃疡病患者或无症状携带者无关，并且不仅与已知毒力因子的表达相关，如细胞毒素相关基因致病岛、空泡毒素A和刘易斯血型抗原。此外，一种或几种未经鉴定的蛋白质，其通过NF-κ B活化起作用，似乎诱导内皮细胞活化。总之，人内皮细胞产生嗜中性粒细胞募集因子，并显示在一定的H刺激后粘附分子表达增加。pylori菌株。这些效应可能有助于中性粒细胞持续募集到H。幽门感染的胃粘膜，也可能导致组织损伤和溃疡形成。
Helicobacter pylori infection causes active chronic inflammation with a continuous recruitment of neutrophils to the inflamed gastric mucosa. To evaluate the role of endothelial cells in this process, we have examined adhesion molecule expression and chemokine and cytokine production from human umbilical vein endothelial cells stimulated with well-characterized H. pylori strains as well as purified proteins. Our results indicate that endothelial cells actively contribute to neutrophil recruitment, since stimulation with H. pylori bacteria induced upregulation of the adhesion molecules VCAM-1, ICAM-1, and E-selectin as well as the chemokines interleukin 8 (IL-8) and growth-related oncogene alpha (GRO-alpha) and the cytokine IL-6. However, there were large variations in the ability of the different H. pylori strains to stimulate endothelial cells. These interstrain variations were seen irrespective of whether the strains had been isolated from patients with duodenal ulcer disease or asymptomatic carriers and were not solely related to the expression of known virulence factors, such as the cytotoxin-associated gene pathogenicity island, vacuolating toxin A, and Lewis blood group antigens. In addition, one or several unidentified proteins which act via NF-kappaB activation seem to induce endothelial cell activation. In conclusion, human endothelial cells produce neutrophil-recruiting factors and show increased adhesion molecule expression after stimulation with certain H. pylori strains. These effects probably contribute to the continuous recruitment of neutrophils to H. pylori-infected gastric mucosa and may also contribute to tissue damage and ulcer formation.