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CXCL16 Regulates Cell-Mediated Immunity toSalmonella entericaSerovar Enteritidis via Promotion of Gamma Interferon Production
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| Zeitschriftentitel: | Infection and Immunity |
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| Personen und Körperschaften: | , , |
| In: | Infection and Immunity, 74, 2006, 12, S. 6885-6894 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Society for Microbiology
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| Schlagwörter: |
| Zusammenfassung: | <jats:title>ABSTRACT</jats:title><jats:p>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<jats:italic>Salmonella enterica</jats:italic>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<jats:italic>S. enteritidis</jats:italic>. 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<jats:italic>S. enteritidis</jats:italic>.</jats:p> |
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| Umfang: | 6885-6894 |
| ISSN: |
0019-9567
1098-5522 |
| DOI: | 10.1128/iai.01065-06 |