Dexamethasone depletes gammadelta T cells and alters the activation state and responsiveness of bovine peripheral blood lymphocyte subpopulations.
Administration of dexamethasone (DEX) to cattle is commonly used in models of stress-induced effects on host defense, including models investigating interactions of microorganisms with their host. Much less is known about the effects of DEX on the adaptive immune response in cattle compared with other species. The objective of the present study was to characterize subsets of circulating lymphocytes in calves before and 48 h after the onset of parenteral DEX treatment. Treatment significantly reduced the overall percentage of circulating lymphocytes and disproportionately depleted the population of gammadeltaTCR(+)/CD8alpha(-) cells. Analysis within the CD8alpha(+) population of T cells revealed that DEX treatment also reduced the CD8alpha(low) subset of gammadeltaT cells coexpressing the activation marker ACT-2(+). By contrast, DEX treatment did not affect the percentage of CD8alpha(low)/CD25(+) cells, indicating that cells with a special activation state were affected. Dexamethasone treatment reduced the number of gammadeltaT cells but increased the percentages of CD14(+) monocytes and activated CD25(+) cells (both CD4(-) and CD4(+)) in peripheral blood mononuclear cell (PBMC) preparations. Although DEX treatment reduced the overall proliferative capacity of PBMC, it enhanced the relative number of proliferating CD4(+) lymphocytes. Lower levels of mRNA for several Th-prototype cytokines (IL-2, IFN-beta, IL-4, transforming growth factor-beta) were detected in short-term PBMC cultures established from DEX-treated calves compared with PBMC cultures from control calves; the amount of il-10 transcripts, however, was unaffected. Results of the study reported here clearly show that DEX treatment does not uniformly suppress the bovine immune system but has differential effects on lymphocyte sub-populations and functions. This information must be considered when using DEX treatment as a bovine stress model.
Menge
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Institute for Hygiene and Infectious Diseases of Animals, Justus-Liebig-University, D-35392 Giessen, Germany. christian.menge@vetmed.uni-giessen.de
Dean-Nystrom
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EA
D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D018414:CD8-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D002417:Cattle; D002418:Cattle Diseases / Q000276:immunology*; D003907:Dexamethasone / Q000494:pharmacology*; D016130:Immunophenotyping / Q000662:veterinary; D007958:Leukocyte Count / Q000662:veterinary; D008213:Lymphocyte Activation / Q000187:drug effects* / Q000276:immunology; D008297:Male; D011897:Random Allocation; D013312:Stress, Physiological / Q000276:immunology / Q000662:veterinary*; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology
D000893:Anti-Inflammatory Agents; D003907:Dexamethasone