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Journal of Dairy Science Vol. 85 No. 3 544-550
© 2002 by American Dairy Science Association ®
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Decreased Neutrophil Function as a Cause of Retained Placenta in Dairy Cattle

Kayoko Kimura 1, Jesse P. Goff 1, Marcus E Kehrli Jr. 1, and Timothy A. Reinhardt 1

1 USDA, Agricultural Research Service National Animal Disease Center Periparturient Disease of Cattle Research Unit Ames, IA 50010-0070

It is unclear why some cows fail to expel the placenta following calving. One theory suggests the fetal placenta must be recognized as "foreign" tissue and rejected by the immune system after parturition to cause expulsion of the placenta. We hypothesized that impaired neutrophil function causes retained placenta (RP). We examined the ability of neutrophils to recognize fetal cotyledon tissue as assessed by a chemotaxis assay, which utilized a placental homogenate obtained from a spontaneously expelled placenta as the chemoattractant. Neutrophil killing ability was also estimated by determining myeloperoxidase activity in isolated neutrophils. Blood samples were obtained from 142 periparturient dairy cattle in two herds. Twenty cattle developed RP (14.1%). Neutrophils isolated from blood of cows with RP had significantly lower neutrophil function in both assays before calving, and this impaired function lasted for 1 to 2 wk after parturition. The addition of antibody directed against interleukin-8 (IL-8) to the cotyledon preparation used as a chemoattractant inhibited chemotaxis by 41%, suggesting that one of the chemoattractants present in the cotyledon at parturition is IL-8. At calving, plasma IL-8 concentration was lower in RP cows (51 ± 12 pg/ml) than in cows expelling the placenta normally (134 ± 11 pg/ml). From these data, we suggest that neutrophil function is a determining factor for the development of RP in dairy cattle. Also, depressed production of IL-8 may be a factor affecting neutrophil function in cows developing RP.

Key Words: chemotaxis • interleukin-8 • periparturient dairy cow • retained placenta

Submitted on September 13, 2001
Accepted on November 16, 2001




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