Submitted to: Journal of Dairy Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 2, 2006
Publication Date: July 20, 2006
Repository URL: http://jds.fass.org/cgi/content/full/89/7/2588
Citation: Kimura, K., Reinhardt, T.A., Goff, J.P. 2006. Parturition and hypocalcemia blunts calcium signals in immune cells of dairy cattle. Journal of Dairy Science. 89(7):2588-2595. Interpretive Summary: Periparturient dairy cows suffer immunosuppression and hypocalcemia. This is a significant economical problem in dairy industry due to increased susceptibility of these cows to infectious diseases. The association between immunosuppression and hypocalcemia has not been characterized. In this study, we clearly show that increased calcium demand during parturition in dairy cows decreases intracellular calcium stores in immune cells. This results in decreased immune function in cows with calcium stress or hypocalcemia. We conclude that the calcium stresses of parturition are, in part, responsible for the immunosuppression these cows suffer and therefore hypocalcemia contributes to increased disease susceptibility of the periparturient cow. Prevention of periparturient immunosuppression can in part be accomplished by prevention of hypocalcemia thus improving cattle health.
Technical Abstract: Since intracellular calcium signaling is a key early feature in immune cell activation, we have hypothesized that the increased demand for calcium in periparturient cows may adversely affect intracellular calcium stores of immune cells. This reduction in intracellular calcium stores in immune cells could blunt intracellular calcium release following an activating stimulus, contributing to the immune suppression seen in these animals. To test this hypothesis, peripheral mononuclear cells were obtained from 27 multiparous dairy cows spanning a period of two weeks before and after parturition. Following activation of these cells by anti-CD3 Ab plus secondary Ab, intracellular calcium release from intracellular stores was measured. The intracellular calcium released in response to the activation signal declined as calcium demand for lactation became more intense and recovered as plasma calcium normalized. Intracellular calcium stores in peripheral mononuclear cells, estimated by pre-treating cells with pervanadate and ionomycin, significantly decreased at parturition and returned to normal levels as the cows’ blood calcium returned to normal levels. Hypocalcemia which is common in periparturient in dairy cows, is associated with decreased intracellular calcium stores in peripheral mononuclear cells. Our data suggest this is the cause of a blunted intracellular calcium release response to an immune cell activation signal. It is concluded that hypocalcemia in the periparturient dairy cow contributes to the immune suppression experienced by these animals and therefore their increased susceptibility to infectious disease.