Journal
MICROBES AND INFECTION
Volume 13, Issue 10, Pages 852-861Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.micinf.2011.04.010
Keywords
Brucella; Endothelial cells; Inflammation mediators; Cytokines; Chemokines; Adhesion molecules
Categories
Funding
- Agencia Nacional de Promocion Cientifica (ANPCYT) [2006-0517, 2006-1335, 2008-0764]
- Universidad de Buenos Aires [UBACYT B015, 20020090100083]
- Consejo Nacional de Investigaciones Cientificas (CONICET)
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available