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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #220519
Title: DEXAMETHASONE DEPLETES GAMMA-DELTA T CELLS AND ALTERS THE ACTIVATION STATE AND RESPONSIVENESS OF BOVINE PERIPHERAL BLOOD LYMPHOCYTE SUBPOPULATIONS

Author
item MENGE, CHRISTIAN - LIEBIG UNIV.GERMANY
item Nystrom, Evelyn

Submitted to: Journal of Dairy Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/14/2008
Publication Date: 6/20/2008
Citation: Menge, C., Nystrom, E.A. 2008. Dexamethasone depletes gamma-delta T cells and alters the activation state and responsiveness of bovine peripheral blood lymphocyte subpopulations. Journal of Dairy Science. 91(6):2284-2298.

Interpretive Summary: Administration of dexamethasone (DEX) to cattle is commonly used in animal models to determine how stress affects host defenses against disease, including models investigating interactions of microorganisms with their host. Much less is known about the effects of DEX on the immune responses in cattle than in other species. The objective of the present study was to characterize subsets of circulating lymphocytes (white blood cells) in calves prior to and 48 h after the onset of intravenously administered DEX treatment. 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 subpopulations and functions. This information must be considered when utilizing DEX treatment to simulate bovine stress-associated disease models.

Technical Abstract: 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 than in other species. The objective of the present study was to characterize subsets of circulating lymphocytes in calves prior to 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 gamma-deltaTCR**+/CD8alpha**- cells. Analysis within the CD8alpha**+ population of T cells revealed that DEX treatment also reduced the CD8alpha**low subset of gamma-deltaT 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. DEX treatment reduced the number of gamma-deltaT cells but increased the numbers of CD14**+ monocytes and activated CD25**+ cells (both CD4**- and CD4**+) in PBMC preparations. Although DEX treatment reduced the overall proliferative capacity of PBMC, it enhanced the relative number of proliferating CD4**+ lymphocytes. Lower levels of mRNAs for several Th-prototype cytokines (IL-2, IFN-gamma, IL-4, TGF-belta) were detected in short term-PBMC cultures established from DEX-treated calves compared to 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 subpopulations and functions. This information must be considered when utilizing DEX treatment to simulate bovine stress-associated disease models.