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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Ruminant Diseases and Immunology Research » Research » Publications at this Location » Publication #162539

Title: GENETIC VARIATION IN BOVINE MONONUCLEAR LEUKOCYTE RESPONSES TO DEXAMETHASONE

Author
item SAAMA, P - MICHIGAN STATE UNIVERSITY
item JACOB, J - MICHIGAN STATE UNIVERSITY
item Kehrli Jr, Marcus
item FREEMAN, A - IOWA STATE UNIVERSITY
item KELM, S - IOWA STATE UNIVERSITY
item KUCK, A - 21ST CENTURY GENETICS
item TEMPELMAN, R - MICHIGAN STATE UNIVERSITY
item BURTON, J - MICHIGAN STATE UNIVERSITY

Submitted to: Journal of Dairy Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/24/2004
Publication Date: 11/1/2004
Citation: Saama, P.M., Jacob, J.B., Kehrli Jr, M.E., Freeman, A.E., Kelm, S.C., Kuck, A.L., Tempelman, R.J., Burton, J.L. 2004. Genetic variation in bovine mononuclear leukocyte responses to dexamethasone. Journal of Dairy Science. 11:3928-37.

Interpretive Summary: Mastitis is an infection of the mammary gland that affects more than half of the dairy cows on over 95% of all dairy farms. On average, U.S. dairy farmers will lose more than $180 per cow annually. Mastitis is a legitimate concern to consumers because of potential antibiotic residues as a result of treating cows for mastitis. The main benefit of the work reported here was the development of a genetic analysis method that can be used with tests of a bull's immune system capacity to resist stress. Bulls with immune systems more resistant to stress will likely be genetically superior for producing offspring who are more resistant to diseases such as mastitis, diarrhea and pneumonia. This technique will be especially useful because we only need to evaluate the immune system of a few bulls. A potential benefit of this research would be less use of antibiotics in cows to treat mastitis through selection of genetically superior breeding stock.

Technical Abstract: The objective of this study was to determine whether bovine mononuclear leukocytes exhibit genetic variability prior to and after a glucocorticoid hormone challenge in vivo. Test animals included 60 pedigreed Holstein bulls treated on 3 consecutive days with dexamethasone and 5 untreated control bulls. Eight indicator traits of leukocyte responsiveness to dexamethasone included the percentages of circulating B cells, T cells (CD4, CD8, and workshop cluster 1 molecule expressed by bovine gamma delta T cell), major histocompatibility complex (MHC) I and II expressing cells, and mean expressions of surface MHC I and MHC II on circulating cells. Blood for this work was collected from each test bull 10 times before, during, and after dexamethasone administration, with corresponding samples taken for control bulls. Random regression models with treatment-specific serial correlation were applied to the leukocyte data sets to estimate genetic and nongenetic sources of variation in baseline and recovery aspects of the traits. All traits responded predictably to glucocorticoid challenge. Genetic variation was observed in baseline measurements of all traits, with heritability estimates ranging from 0.21 +/- 0.03 to 0.60 +/- 0.06. Genetic variation in linear recovery from nadir values following dexamethasone administration was significant only for percentage CD4, percentage CD8, and for surface expression of MHC II. The genetic covariance between basal and linear recovery was positive and significant for percentage CD4, percentage CD8, and MHC II expression. The bovine lymphocyte antigen DRB3.2 locus accounted for significant proportions of total variation in percentage MHC II cells and MHC I expression. These results suggest that genetic variability exists for important basal and glucocorticoid-modified phenotypes of bovine mononuclear leukocytes, implying that immunocompetence traits impacted by this stress hormone may be enhanced by genetic selection.