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BvrR/BvrS-controlled outer membrane proteins Omp3a and Omp3b are not essential for Brucella abortus virulence
dc.creator | Manterola, Lorea | es_ES |
dc.creator | Guzman-Verri, Caterina | es_ES |
dc.creator | Chaves Olarte, Esteban | es_ES |
dc.creator | Barquero-Calvo, Elías | es_ES |
dc.creator | Miguel, María Jesús de | es_ES |
dc.creator | Moriyón Uría, Ignacio | es_ES |
dc.creator | Grilló Dolset, María Jesús | es_ES |
dc.creator | López Goñi, Ignacio | es_ES |
dc.creator | Moreno, Edgardo | es_ES |
dc.date.accessioned | 2019-01-23T11:16:17Z | |
dc.date.available | 2019-01-23T11:16:17Z | |
dc.date.issued | 2007 | |
dc.identifier.issn | 0019-9567 (Print) | |
dc.identifier.issn | 1098-5522 (Electronic) | |
dc.identifier.uri | https://hdl.handle.net/2454/32077 | |
dc.description.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 ranges similar to those of the wild-type (WT) counterpart. Likewise, omp3a and omp3b mutants 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 the omp3a mutant generated slightly higher levels of tumor necrosis factor alpha than the WT, whereas the bvrS mutant induced lower levels of this cytokine. Since the 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 Omps. | en |
dc.description.sponsorship | This work was partially supported by grant 8-N-2005 from NeTropica; grants from the MICIT/CONICIT, Costa Rica; a grant from Florida Ice & Farm; FIDA from the Universidad Nacional (UNA); and FS from the CONARE UNA/UCR agreement. Other grants were from the IFS (B/3456-1 and B/3456-2), the MEC of Spain (AGL2004-01162 and BIO2005-04985), and RTIC del FIS (objetivo 2, 2000-2006, G03/204). Fellowship support to L. Manterola from the Gobierno Vasco is gratefully acknowledged. | en |
dc.format.extent | 8 p. | |
dc.format.mimetype | application/pdf | en |
dc.language.iso | eng | en |
dc.publisher | American Society for Microbiology | en |
dc.relation.ispartof | Infection and immunity, vol. 75, nº 10, oct. 2007, p. 4867–4874 | en |
dc.rights | © 2007, American Society for Microbiology. All Rights Reserved. | en |
dc.subject | Brucella abortus pathogenicity | en |
dc.subject | Virulence genetics | en |
dc.title | BvrR/BvrS-controlled outer membrane proteins Omp3a and Omp3b are not essential for Brucella abortus virulence | en |
dc.type | info:eu-repo/semantics/article | en |
dc.type | Artículo / Artikulua | es |
dc.contributor.department | IdAB. Instituto de Agrobiotecnología / Agrobioteknologiako Institutua | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | en |
dc.rights.accessRights | Acceso abierto / Sarbide irekia | es |
dc.identifier.doi | 10.1128/iai.00439-07 | |
dc.relation.publisherversion | https://doi.org/10.1128/iai.00439-07 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | en |
dc.type.version | Versión publicada / Argitaratu den bertsioa | es |