Proinflammatory response of human endothelial cells to Brucella infection
Proinflammatory response of human endothelial cells to Brucella infection
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DOI：
10.1016/j.micinf.2011.04.010
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发表时间：
2011-09-01
影响因子：
5.8
通讯作者：
Baldi, Pablo C.
中科院分区：
文献类型：
--
作者：
Ferrero, Mariana C.;Bregante, Julieta;Baldi, Pablo C.
尽管布鲁氏菌病患者的血管病变如脉管炎、心内膜炎和霉菌性动脉瘤已被描述，但布鲁氏菌与内皮细胞的相互作用尚未被描述。在本研究中，我们发现流产布鲁氏菌和猪布鲁氏菌可以在原代人脐静脉内皮细胞(HUVEC)和微血管内皮细胞系HMEC-1中感染和复制。感染后HUVEC和HMEC-1细胞产生IL-8、MCP-1和IL-6，黏附分子(HUVEC和HUVEC均表达CD54，HUVEC表达CD106和CD62E)增加。用从细菌外膜提纯的抗原进行的实验表明，脂蛋白(Omp19)而不是脂多糖介导了这些促炎反应。极化的HMEC-1细胞感染后，其促进中性粒细胞从单层根尖向基底侧迁移的能力增强，而在基底侧用活细菌刺激细胞时，也观察到同样的现象。总体而言，这些结果表明布鲁氏菌属。可感染内皮细胞并在内皮细胞内存活，并可诱导促炎反应，这可能与布鲁氏菌病的血管表现有关。(C)2011年巴斯德研究所。爱思唯尔·马森公司出版。版权所有。
Although vascular pathologies such as vasculitis, endocarditis and mycotic aneurysms have been described in brucellosis patients, the interaction of Brucella with the endothelium has not been characterized. In this study we show that Brucella abortus and Brucella suis can infect and replicate in primary human umbilical vein endothelial cells (HUVEC) and in the microvascular endothelial cell line HMEC-1. Infection led to an increased production of IL-8, MCP-1 and IL-6 in HUVEC and HMEC-1 cells, and an increased expression of adhesion molecules (CD54 in both cells, CD106 and CD62E in HUVEC). Experiments with purified antigens from the bacterial outer membrane revealed that lipoproteins (Omp19) but not lipopolysaccharide mediate these proinflammatory responses. Infection of polarized HMEC-1 cells resulted in an increased capacity of these cells to promote the transmigration of neutrophils from the apical to the basolateral side of the monolayer, and the same phenomenon was observed when the cells were stimulated with live bacteria from the basolateral side. Overall, these results suggest that Brucella spp. can infect and survive within endothelial cells, and can induce a proinflammatory response that might be involved in the vascular manifestations of brucellosis. (C) 2011 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.