Abstract
Reduced antigen-specific CD8+ T cell responses as a result of increased bacterial translocation in chronic ethanol consuming mice (129.17)
The Journal of immunology (1950), Vol.182(1_Supplement), pp.129-129.17
04/01/2009
DOI: 10.4049/jimmunol.182.Supp.129.17
Abstract
Abstract Chronic ethanol consumption leads to increased translocation of bacterial products such as LPS and PGN. Previously, we have shown that chronic ethanol consumption results in reduced antigen-specific CD8+ T cell responses following attenuated Listeria monocytogenes (actA-LM) inoculation. We hypothesized that reduced antigen-specific CD8+ T cell response in chronic ethanol mice can be modeled by treatment with bacterial products. Control water mice were pretreated with either LPS or TLR-2 agonist to mimic systemic bacterial product translocation and their response to actA-LM inoculation was evaluated. Antigen-specific CD8+ T cell responses to actA- LM were reduced in Pam3CSK4 or LPS treated mice, similar to ethanol mice. Further analyses showed that the reduction of antigen-specific CD8+ T cells in TLR agonist treated mice was due to an indirect effect on antigen presenting cells, as well as a direct effect on CD8+ T cells. None of the TLR agonist effects on CD8+ T cells was reversed by prior depletion of natural Treg cells, or by the depletion of all CD4+ T cells, nor was the reduction of IL2Rb reversed by several days in culture. Reduction of antigen-specific CD8+ T cells was also independent of IL-10. The data as a whole clearly indicate that TLR agonists resulting from bacterial translocation represent one potent mechanism for alteration of antigen-specific CD8+ T cell responses.
Details
- Title: Subtitle
- Reduced antigen-specific CD8+ T cell responses as a result of increased bacterial translocation in chronic ethanol consuming mice (129.17)
- Creators
- Prajwal GurungBetty M YoungLucas E TurnerRuth A ColemanSusan WiechertThomas J WaldschmidtKevin L LeggeRobert T Cook
- Resource Type
- Abstract
- Publication Details
- The Journal of immunology (1950), Vol.182(1_Supplement), pp.129-129.17
- DOI
- 10.4049/jimmunol.182.Supp.129.17
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Language
- English
- Date published
- 04/01/2009
- Academic Unit
- Pathology; Microbiology and Immunology; Infectious Diseases; Internal Medicine
- Record Identifier
- 9984362753002771
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