Genetic variation in bovine mononuclear leukocyte responses to dexamethasone.
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 gammadelta 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.
Saama
P M
PM
Department of Animal Science, Michigan State University, East Lansing 48824, USA.
Jacob
J B
JB
Kehrli
M E
ME
Freeman
A E
AE
Kelm
S C
SC
Kuck
A L
AL
Tempelman
R J
RJ
Burton
J L
JL
D000818:Animals; D002417:Cattle / Q000235:genetics* / Q000276:immunology; D003907:Dexamethasone / Q000494:pharmacology*; D014644:Genetic Variation; D005938:Glucocorticoids / Q000494:pharmacology*; D015395:Histocompatibility Antigens Class I / Q000032:analysis / Q000378:metabolism; D000949:Histocompatibility Antigens Class II / Q000032:analysis / Q000378:metabolism; D016130:Immunophenotyping; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000276:immunology; D008297:Male; D019655:Quantitative Trait, Heritable; D012044:Regression Analysis
D005938:Glucocorticoids; D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II; D003907:Dexamethasone