Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice
Autor: | Sergio C. Oliveira, Vasco Azevedo, Gilson Costa Macedo, Ana Paula Macedo de Souza Brandão, Leda Quercia Vieira, Natalia B. Carvalho, Fernanda S. Oliveira |
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Jazyk: | angličtina |
Rok vydání: | 2011 |
Předmět: |
lcsh:Immunologic diseases. Allergy
Article Subject Immunology Brucella abortus Spleen Brucella Biology Brucellosis Interferon-gamma Mice Immune system medicine Immunology and Allergy Animals Humans Interferon gamma Genetic Predisposition to Disease Mice Knockout Intracellular parasite Macrophages Interferon-alpha General Medicine biology.organism_classification Virology Interleukin-12 Mice Inbred C57BL medicine.anatomical_structure Knockout mouse Interleukin 12 lcsh:RC581-607 beta 2-Microglobulin CD8 medicine.drug Research Article |
Zdroj: | Clinical and Developmental Immunology Clinical and Developmental Immunology, Vol 2012 (2012) |
ISSN: | 1740-2530 1740-2522 |
Popis: | Brucella abortusis 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 againstB. abortus. Herein, IFN-γand IL-12/β2-microglobulin (β2-m) knockout mice were used to determine whether CD8+ T cells and IL-12-dependent IFN-γdeficiency would be more critical to controlB. abortusinfection compared to the lack of endogenous IFN-γ. At 1 week after infection, IFN-γKO and IL-12/β2-m KO mice showed increased numbers of bacterial load in spleens; however, at 3 weeks postinfection (p.i.), only IFN-γKO succumbed toBrucella. All IFN-γKO 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 toBrucellawas associated to undetectable levels of IFN-γin mouse splenocytes and inability of these cells to lyseBrucella-infected macrophages. However, the lack of endogenous IFN-γwas found to be more important to control brucellosis than CD8+ T cells and IL-12-dependent IFN-γdeficiencies. |
Databáze: | OpenAIRE |
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