Inactivation of formyltransferase (wbkC) gene generates a Brucella abortus rough strain that is attenuated in macrophages and in mice |
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Authors: | Thaí s Lourdes Santos Lacerda,Patrí cia Gomes Cardoso,Leonardo Augusto de Almeida,Ilana Lopes Baratella da Cunha Camargo,Daniela Almeida Freitas Afonso,Cyntia Cardoso Trant,Gilson Costa Macedo,Eleonora Campos,Silvio L. Cravero,Suzana P. Salcedo,Jean-Pierre Gorvel,Sé rgio Costa Oliveira |
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Affiliation: | 1. Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil;2. Department of Biology, Federal University of Lavras, Lavras, Brazil;3. Department of Physics and Informatic, Physics Institute of São Carlos, University of São Paulo, São Carlos, Brazil;4. Instituto de Biotecnologia, INTA-Castelar, Castelar, Buenos Aires, Argentina;5. Centre d’Immunologie de Marseille-Luminy, Aix Marseille Université, Faculté de Sciences de Luminy, Marseille, France;6. INSERM, U631, Marseille, France;g CNRS, UMR6102, Marseille, France |
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Abstract: | Rough mutants of Brucella abortus were generated by disruption of wbkC gene which encodes the formyltransferase enzyme involved in LPS biosynthesis. In bone marrow-derived macrophages the B. abortusΔwbkC mutants were attenuated, could not reach a replicative niche and induced higher levels of IL-12 and TNF-α when compared to parental smooth strains. Additionally, mutants exhibited attenuation in vivo in C57BL/6 and interferon regulatory factor-1 knockout mice. ΔwbkC mutant strains induced lower protective immunity in C56BL/6 than smooth vaccine S19 but similar to rough vaccine RB51. Finally, we demonstrated that Brucella wbkC is critical for LPS biosynthesis and full bacterial virulence. |
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Keywords: | Brucella abortus Rough strain Live vaccine |
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