|Kehrli Jr, Marcus|
|Reinhardt, Timothy - Tim|
Submitted to: Journal of Dairy Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/28/2001
Publication Date: N/A
Citation: Interpretive Summary: Retained placenta is a disorder of dairy cows characterized by a failure to expel the fetal placenta shortly after calving. The presence of this material in the cow's uterus often causes an infection of the uterus and reduces fertility of the cow. The cause of retained placenta is unknown. Prevailing theories suggest that retained placenta is caused by hormone imbalance, but numerous studies have failed to provide insight as to which hormones are responsible for causing retained placenta. We tested the hypothesis that the immune system plays a role in retained placenta. This theory involves recognition of the fetal placenta as foreign tissue to the cow after delivery of the calf. We hypothesized that the white blood cells of the cow, specifically the neutrophils, must recognize and attack the fetal placenta if normal expulsion of the placenta is to occur. We observed that neutrophils of cows with retained placenta do not recognize placenta as well as neutrophils of normal cows and further that these neutrophils have less capacity to kill bacteria than do neutrophils of cows that do not develop retained placenta. These data supply evidence that a poorly functioning immune system is the reason why some cows develop a retained placenta. Management schemes and nutritional strategies aimed at improving immune function at calving could help eliminate retained placenta in dairy cattle, which would be of significant value to dairy producers worldwide.
Technical Abstract: 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 2 herds. Twenty cattle developed RP (14.1%). Neutrophils isolated from blood of cows with RP had significantly lower neutrophil function in both assays prior to calving and this impaired function lasted for 1-2 wk after parturition. Addition of antibody directed against interleukin-8 (IL-8) to the cotyledon preparation used as a chemoattractant inhibited hemotaxis by 41%, suggesting 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). These data suggest neutrophil function determines whether or not the cow will develop RP. These data also suggest that depressed production of IL-8 may be a factor affecting neutrophil function in cows developing RP.