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Infect. Immun. doi:10.1128/IAI.00439-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The BvrR/BvrS-controlled outer membrane proteins Omp3a and Omp3b are not essential for Brucella abortus virulence

Departamento de Microbiología y Parasitología, Universidad de Navarra, 31008 Pamplona, Spain; Programa de Investigación en Enfermedades Tropicales (PIET), Escuela de Medicina Veterinaria, Universidad Nacional, 304-3000 Heredia, Costa Rica; Centro de Investigación en Enfermedades Tropicales, Facultad de Microbiología, Universidad de Costa Rica, 1000 San José, Costa Rica

^* To whom correspondence should be addressed. Email: catguz{at}medvet.una.ac.cr.

	Abstract

The Brucella abortus two component regulatory system BvrR/BvrS controls the expression of outer membrane proteins (Omp) Omp3a (Omp25) and Omp3b (Omp22). Disruption of bvrS or bvrR generates avirulent mutants with altered cell permeability, higher sensitivity to microbicidal peptides and complement. Consequently, the role of Omp3a and Omp3b in virulence was examined. Similar to bvrS- or bvrR- mutants, omp3a- and omp3b- mutants displayed increased attachment to cells indicating surface alterations. However, they showed unaltered permeability, normal expression of Omp10, Omp16, Omp19, Omp2b and Omp1, native hapten polysaccharide and lipopolysaccharide and were resistant to complement and polymyxin B at similar ranges as the wild type (WT) counterpart. Likewise, omp3a- and omp3b- were able to replicate in murine macrophages and in HeLa cells, were resistant to the killing action of human neutrophils and persisted in mice like the WT strain. Murine macrophages infected with omp3a- generated slightly higher levels of TNF- as compared to the WT, whereas bvrS- induced lower levels of this cytokine. Since absence of Omp3a or Omp3b does not result in attenuation, it can be concluded that BvrR/BvrS influences additional Brucella properties involved in virulence. Our results are discussed in the light of previous works suggesting that disruption of omp3a generates attenuated Brucella strains and we speculate on the role of group 3 Omp.