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

Abstract EN

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.