title: Depressed DHEA and increased sickness response behaviors in lame dairy cows with inflammatory foot lesions.
abstract: Lameness is a multifactorial condition influenced by the environment, genetics, management and nutrition. Detection of lameness is subjective and currently limited to visual locomotion observations which lack reliability and sensitivity. The objective of this study was to search for potential biomarkers of inflammatory foot lesions that underlie most cases of lameness in dairy cows, with a focus on the sickness response and relevant endocrine, immune and behavioral changes. Serum and peripheral blood mononuclear cells (PBMC) were collected from eight sound and eight lame high-producing Holstein cows. Immune cell activation was investigated in PBMCs using a candidate gene approach in which the expression of pro-opiomelanocortin, interleukin-1beta, l-selectin, matrix metalloproteinase-9 and glucocorticoid receptor-alpha was measured via quantitative real time-RT-PCR. Endocrine changes were investigated by monitoring serum concentrations of cortisol and dehydroepiandrosterone (DHEA). Additionally, systematic behavioral observations were carried out to characterize a behavioral profile associated with a sickness response typical of this condition. Lame cows showed significantly lower eating (P=0.01) and ruminating (P=0.01) behaviors and higher incidence of self-grooming (P=0.04) compared to sound cows. Lame cows also showed a 23% decrease in serum DHEA (P=0.01) and 65% higher cortisol:DHEA ratio (P=0.06) compared to sound cows. However, no significant differences were found in candidate gene expression between lame and sound cows. In association with sickness behaviors, serum DHEA concentration and cortisol:DHEA ratio are promising objective indicators of inflammatory foot lesions in dairy cattle and may be useful as diagnostic targets for animals in need of treatment.
authors.affiliation: Immunogenetics Laboratory, Department of Animal Science, Michigan State University, East Lansing, MI 48824, USA.
authors.forename: P E
authors.initials: PE
authors.lastname: Almeida
authors.forename: P S D
authors.initials: PS
authors.lastname: Weber
authors.forename: J L
authors.initials: JL
authors.lastname: Burton
authors.forename: A J
authors.initials: AJ
authors.lastname: Zanella
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D002417:Cattle; D002418:Cattle Diseases / Q000097:blood / Q000235:genetics / Q000276:immunology / Q000503:physiopathology*; D003687:Dehydroepiandrosterone / Q000097:blood*; D005260:Female; D005534:Foot Diseases / Q000235:genetics / Q000276:immunology / Q000503:physiopathology / Q000662:veterinary*; D015870:Gene Expression; D006854:Hydrocortisone / Q000097:blood*; D053583:Interleukin-1beta / Q000097:blood / Q000235:genetics; D019041:L-Selectin / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D007794:Lameness, Animal / Q000097:blood / Q000235:genetics / Q000276:immunology / Q000503:physiopathology*; D007963:Leukocytes, Mononuclear / Q000276:immunology; D020780:Matrix Metalloproteinase 9 / Q000097:blood / Q000235:genetics; D011333:Pro-Opiomelanocortin / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000097:blood / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary
chemical_list: D053583:Interleukin-1beta; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; C411470:glucocorticoid receptor alpha; D019041:L-Selectin; D003687:Dehydroepiandrosterone; D011333:Pro-Opiomelanocortin; D020780:Matrix Metalloproteinase 9; D006854:Hydrocortisone