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1 Department of Biomedical Sciences, Iowa State University, Ames 50010
2 USDA, Agricultural Research Service, National Animal Disease Center, Metabolic Diseases and Immunology Research Unit, Ames, IA 50010-0070
Neutrophil function is reduced in periparturient dairy cows. Possible factors that reduce neutrophil function include endocrine changes associated with parturition and metabolic stresses associated with lactogenesis. In this study, mastectomized and intact cows were studied to specifically examine the effects of lactogenesis on neutrophil function in periparturient cows. Expression of adhesion molecules on neutrophils (L-selectin, mediating capture and rolling adhesion, and ß2- integrin, mediating tight adhesion vital to egress) and neutrophil myeloperoxidase activity (an index of bactericidal activity) were assessed in mastectomized and intact cows. Expression of L-selectin decreased at parturition followed by rapid recovery to prepartum values in both intact and mastectomized cows. Expression of ß2-integrins increased in intact cows at parturition but not in mastectomized cows. Expression of ß2-integrins was greater in intact cows than in mastectomized cows throughout the study. Neutrophil myeloperoxidase activity decreased from baseline prepartum values as parturition approached in both intact and mastectomized cows, which suggests the endocrine changes associated with the act of parturition are predominant factors causing loss of neutrophil function. Myeloperoxidase activity recovered to prepartum values within a week of parturition in mastectomized cows; however, myeloperoxidase activity remained depressed in neutrophils obtained from intact cows throughout the first 20 d of lactation. The presence of the mammary gland and its attendant metabolic stresses slowed recovery of neutrophil function, which suggests that the metabolic stress of lactation exacerbated periparturient immunosuppression.
Key Words: periparturient immunosuppression ßbeta;2-integrin L-selectin myeloperoxidase
Submitted on January 7, 1999
Accepted on June 7, 1999
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