Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice

Brucella abortus is a facultative intracellular bacterial pathogen that causes abortion in domestic animals and undulant fever in humans. IFN-γ, IL-12, and CD8+ T lymphocytes are important components of host immune responses against B. abortus. Herein, IFN-γ and IL-12/β2-microglobulin (β2-m) knockou...

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Main Authors: Ana Paula M. S. Brandão, Fernanda S. Oliveira, Natalia B. Carvalho, Leda Q. Vieira, Vasco Azevedo, Gilson C. Macedo, Sergio C. Oliveira
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Clinical and Developmental Immunology
Online Access:http://dx.doi.org/10.1155/2012/589494
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author Ana Paula M. S. Brandão
Fernanda S. Oliveira
Natalia B. Carvalho
Leda Q. Vieira
Vasco Azevedo
Gilson C. Macedo
Sergio C. Oliveira
author_facet Ana Paula M. S. Brandão
Fernanda S. Oliveira
Natalia B. Carvalho
Leda Q. Vieira
Vasco Azevedo
Gilson C. Macedo
Sergio C. Oliveira
author_sort Ana Paula M. S. Brandão
collection DOAJ
description Brucella abortus is a facultative intracellular bacterial pathogen that causes abortion in domestic animals and undulant fever in humans. IFN-γ, IL-12, and CD8+ T lymphocytes are important components of host immune responses against B. abortus. Herein, IFN-γ and IL-12/β2-microglobulin (β2-m) knockout mice were used to determine whether CD8+ T cells and IL-12-dependent IFN-γ deficiency would be more critical to control B. abortus infection compared to the lack of endogenous IFN-γ. At 1 week after infection, IFN-γ KO and IL-12/β2-m KO mice showed increased numbers of bacterial load in spleens; however, at 3 weeks postinfection (p.i.), only IFN-γ KO succumbed to Brucella. All IFN-γ KO had died at 16 days p.i. whereas death within the IL-12/β2-m KO group was delayed and occurred at 32 days until 47 days postinfection. Susceptibility of IL-12/β2-m KO animals to Brucella was associated to undetectable levels of IFN-γ in mouse splenocytes and inability of these cells to lyse Brucella-infected macrophages. However, the lack of endogenous IFN-γ was found to be more important to control brucellosis than CD8+ T cells and IL-12-dependent IFN-γ deficiencies.
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spelling doaj-art-5f29e6084eee42b88007363e62f711ee2025-02-03T01:27:16ZengWileyClinical and Developmental Immunology1740-25221740-25302012-01-01201210.1155/2012/589494589494Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient MiceAna Paula M. S. Brandão0Fernanda S. Oliveira1Natalia B. Carvalho2Leda Q. Vieira3Vasco Azevedo4Gilson C. Macedo5Sergio C. Oliveira6Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901 Belo Horizonte, MG, BrazilDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901 Belo Horizonte, MG, BrazilDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901 Belo Horizonte, MG, BrazilDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901 Belo Horizonte, MG, BrazilDepartment of General Biology, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901 Belo Horizonte, MG, BrazilDepartment of Parasitology, Microbiology and Immunology, Biological Sciences Institute, Federal University of Juiz de Fora, 36036-900 Juiz de Fora, MG, BrazilDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901 Belo Horizonte, MG, BrazilBrucella abortus is a facultative intracellular bacterial pathogen that causes abortion in domestic animals and undulant fever in humans. IFN-γ, IL-12, and CD8+ T lymphocytes are important components of host immune responses against B. abortus. Herein, IFN-γ and IL-12/β2-microglobulin (β2-m) knockout mice were used to determine whether CD8+ T cells and IL-12-dependent IFN-γ deficiency would be more critical to control B. abortus infection compared to the lack of endogenous IFN-γ. At 1 week after infection, IFN-γ KO and IL-12/β2-m KO mice showed increased numbers of bacterial load in spleens; however, at 3 weeks postinfection (p.i.), only IFN-γ KO succumbed to Brucella. All IFN-γ KO had died at 16 days p.i. whereas death within the IL-12/β2-m KO group was delayed and occurred at 32 days until 47 days postinfection. Susceptibility of IL-12/β2-m KO animals to Brucella was associated to undetectable levels of IFN-γ in mouse splenocytes and inability of these cells to lyse Brucella-infected macrophages. However, the lack of endogenous IFN-γ was found to be more important to control brucellosis than CD8+ T cells and IL-12-dependent IFN-γ deficiencies.http://dx.doi.org/10.1155/2012/589494
spellingShingle Ana Paula M. S. Brandão
Fernanda S. Oliveira
Natalia B. Carvalho
Leda Q. Vieira
Vasco Azevedo
Gilson C. Macedo
Sergio C. Oliveira
Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice
Clinical and Developmental Immunology
title Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice
title_full Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice
title_fullStr Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice
title_full_unstemmed Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice
title_short Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice
title_sort host susceptibility to brucella abortus infection is more pronounced in ifn γ knockout than il 12 β2 microglobulin double deficient mice
url http://dx.doi.org/10.1155/2012/589494
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