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|Title:||CXCL16 regulates cell-mediated immunity to Salmonella enterica serovar Enteritidis via promotion of gamma interferon production|
|Citation:||Infection and Immunity, 2006; 74(12):6885-6894|
|Publisher:||Amer Soc Microbiology|
|Olivier L. Fahy, Scott L. Townley, and Shaun R. McColl|
|Abstract:||CXCL16 is a recently discovered multifaceted chemokine that has been shown not only to recruit activated T lymphocytes but also to play a direct role in the binding and phagocytosis of bacteria by professional antigen-presenting cells. In this study, we investigated the role of CXCL16 in vivo in the regulation of the immune response using a murine model of Salmonella enterica serovar Enteritidis infection. The expression of CXCL16 was strongly upregulated in the spleens and livers of animals developing an immune response to a primary acute infection but not in the Peyer's patches. Animals developing a secondary response after reexposure to the bacteria displayed a similar pattern of expression. During the primary response, prior treatment with neutralizing antibodies to CXCL16 induced a significant increase in bacterial burden in the spleen and liver. The production of gamma interferon (IFN-γ) by the lymphocytes in the spleen was decreased by anti-CXCL16 treatment. In comparison, during the secondary response, anti-CXCL16 treatment also significantly increased bacterial burden in both the spleen and liver but had no effect on IFN-γ production. No role was found for CXCL16 in the production of antibody against SefA, a major surface antigen of S. enteritidis. Together, these results demonstrate a role for CXCL16 in the control of bacterial colonization of target organs and, more specifically, in the regulation of the cell-mediated arm of the primary response to S. enteritidis.|
Mice, Inbred BALB C
|Description:||Copyright © 2006, American Society for Microbiology|
|Appears in Collections:||Aurora harvest|
Molecular and Biomedical Science publications
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