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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2012-01-01
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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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id | doaj-art-5f29e6084eee42b88007363e62f711ee |
institution | Kabale University |
issn | 1740-2522 1740-2530 |
language | English |
publishDate | 2012-01-01 |
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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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