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Murine and bovine ?? T cells enhance innate immunity against Brucella abortus infections.

ABSTRACT: ?? T cells have been postulated to act as a first line of defense against infectious agents, particularly intracellular pathogens, representing an important link between the innate and adaptive immune responses. Human ?? T cells expand in the blood of brucellosis patients and are active against Brucella in vitro. However, the role of ?? T cells in vivo during experimental brucellosis has not been studied. Here we report TCR?(-/-) mice are more susceptible to B. abortus infection than C57BL/6 mice at one week post-infection as measured by splenic colonization and splenomegaly. An increase in TCR?? cells was observed in the spleens of B. abortus-infected C57BL/6 mice, which peaked at two weeks post-infection and occurred concomitantly with diminished brucellae. ?? T cells were the major source of IL-17 following infection and also produced IFN-?. Depletion of ?? T cells from C57BL/6, IL-17R?(-/-), and GMCSF(-/-) mice enhanced susceptibility to B. abortus infection although this susceptibility was unaltered in the mutant mice; however, when ?? T cells were depleted from IFN-?(-/-) mice, enhanced susceptibility was observed. Neutralization of ?? T cells in the absence of TNF-? did not further impair immunity. In the absence of TNF-? or ?? T cells, B. abortus-infected mice showed enhanced IFN-?, suggesting that they augmented production to compensate for the loss of ?? T cells and/or TNF-?. While the protective role of ?? T cells was TNF-?-dependent, ?? T cells were not the major source of TNF-? and activation of ?? T cells following B. abortus infection was TNF-?-independent. Additionally, bovine TCR?? cells were found to respond rapidly to B. abortus infection upon co-culture with autologous macrophages and could impair the intramacrophage replication of B. abortus via IFN-?. Collectively, these results demonstrate ?? T cells are important for early protection to B. abortus infections.

SUBMITTER: Skyberg JA

PROVIDER: S-EPMC3134454 | biostudies-other | 2011

REPOSITORIES: biostudies-other

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Murine and bovine γδ T cells enhance innate immunity against Brucella abortus infections.

Skyberg Jerod A JA Thornburg Theresa T Rollins Maryclare M Huarte Eduardo E Jutila Mark A MA Pascual David W DW

PloS one 20110712 7

γδ T cells have been postulated to act as a first line of defense against infectious agents, particularly intracellular pathogens, representing an important link between the innate and adaptive immune responses. Human γδ T cells expand in the blood of brucellosis patients and are active against Brucella in vitro. However, the role of γδ T cells in vivo during experimental brucellosis has not been studied. Here we report TCRδ(-/-) mice are more susceptible to B. abortus infection than C57BL/6 mic ...[more]

PMID: 21765931

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Project description:Brucellosis is still a widespread zoonotic disease. Very little is known about the interaction between B. abortus and trophoblastic cells, which is essential for better understanding the pathogenesis of the Brucella-induced placentitis and abortion, a key event for transmission of the disease. The goal of this study was to evaluate the profile of gene expression by bovine trophoblastic cells during infection with B abortus. Explants of chorioallantoic membranes were inoculated with B. abortus strain 2308. Microarray analysis was performed at 4 h after infection, and expression of cytokines and chemokines by trophoblastic cells was assessed by real time RT-PCR at 6 and 12 h after inoculation. In addition, cytokine and chemokine expression was evaluated in placentomes from experimentally infected cows. Expression of pro-inflammatory genes by trophoblastic cells was suppressed at 4 h after inoculation, whereas a significant up-regulation of CXC chemokines, namely CXCL6 (GCP-2) and CXCL8 (IL-8), was observed at 12, but not at 6 h after inoculation. Placentomes of experimentally infected cows had a similar profile of chemokine expression, with upregulation of CXCL6 and CXCL8. Our data indicate that B. abortus modulates the innate immune response by trophoblastic cells, suppressing expression of pro-inflammatory mediators during the early stages of infection that is followed by a delayed and mild expression of pro-inflammatory chemokines, which is similar to the profile of chemokine expression in the placentomes of experimentally infected cows. This trophoblastic response is likely to contribute to the pathogenesis of B. abortus-induced placentitis. Keywords: trophoblast response to Brucella Total RNA used for microarray analysis was obtained from 6 placentas with 12 infected and 12 control explants from each placenta. At 4 h after inoculation, total RNA was isolated from the trophoblastic surface of the explants. Three RNA pools from two placentas each were generated prior to cDNA synthesis.

Dataset Information

Murine and bovine ?? T cells enhance innate immunity against Brucella abortus infections.

Publications

Murine and bovine γδ T cells enhance innate immunity against Brucella abortus infections.

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