Mastitis is one of the most prevalent diseases in cattle and remains among the most costly diseases to the dairy industry. Various surveys have indicated a greater prevalence of and risk for mastitis in Holstein cows than in Jersey cows. The innate immune system comprises the immediate host defense mechanisms that respond to infection, and differences in the magnitude and rapidity of this response are known to influence susceptibility to and clearance of infectious pathogens. The reported differences in the prevalence of mastitis between Holstein and Jersey cows may suggest the occurrence of breed-dependent differences in the innate immune response to intramammary infection. The objective of the current study was to compare the acute phase and cytokine responses of Holstein and Jersey cows following intramammary infection by the bacterial pathogen Escherichia coli, a leading cause of clinical mastitis. All cows in the study were in similar stages of lactation, of the same parity, subjected to the same housing and management conditions, and experimentally infected on the same day with the same inoculum preparation. Before and after infection, the following innate immune parameters were monitored: bacterial clearance; febrile response; induction of the acute phase proteins serum amyloid A and lipopolysaccharide-binding protein; alterations in total and differential white blood cell counts; changes in milk somatic cell counts and mammary vascular permeability; and induction of the cytokines IFN-gamma, IL-1beta, IL-8, IL-12, and tumor necrosis factor-alpha. Overall innate immune responses were similar between the 2 breeds; however, temporal differences in the onset, cessation, and duration of several responses were detected. Despite these differences, intramammary clearance of E. coli was comparable between the breeds. Together, these data demonstrate a highly conserved innate immune response of Holstein and Jersey cows to E. coli intramammary infection.
1,25-Dihydroxyvitamin D-24-hydroxylase (24-hydroxylase) modulates the biological effects of 1,25-dihydroxyvitamin D [1,25-(OH)2D] in tissues. The presence of 24-hydroxylase in intestinal mucosa and the mass of the intestine suggest that the intestine is a major site of catabolism of 1,25-(OH)2D. How intestinal levels of 24-hydroxylase are regulated under various dietary conditions, such as calcium (Ca) or phosphorus (P) restriction, is poorly understood. In a series of trials on weanling and mature rats, the effects of dietary Ca or P restriction were compared with the effects of exogenous 1,25-(OH)2D3 administration on intestinal 24-hydroxylase activity. Exogenous administration of 1,25-(OH)2D3, by single bolus injection or constant infusion, increased intestinal 24-hydroxylase activity significantly. Dietary Ca and P restriction both resulted in increased plasma 1,25-(OH)2D3 concentrations several-fold above control rat values (P less than 0.001) and to levels higher than those achieved by constant infusion of 1.3 ng 1,25-(OH)2D3/h. Dietary Ca restriction increased intestinal 24-hydroxylase 6- to 20-fold above that of rats fed a Ca-replete diet (P less than 0.001). Dietary P restriction had no significant effect on intestinal 24-hydroxylase activity. These data suggest that dietary Ca restriction results in increased plasma levels of 1,25-(OH)2D3, which, in turn, leads to up-regulation of intestinal 24-hydroxylase. Conversely, dietary P restriction prevents 1,25-(OH)2D3-mediated up-regulation of 24-hydroxylase.
1,25-Dihydroxyvitamin D-24-hydroxylase (24-hydroxylase) modulates the biological effects of 1,25-dihydroxyvitamin D [1,25-(OH)2D] in tissues. The presence of 24-hydroxylase in intestinal mucosa and the mass of the intestine suggest that the intestine is a major site of catabolism of 1,25-(OH)2D. How intestinal levels of 24-hydroxylase are regulated under various dietary conditions, such as calcium (Ca) or phosphorus (P) restriction, is poorly understood. In a series of trials on weanling and mature rats, the effects of dietary Ca or P restriction were compared with the effects of exogenous 1,25-(OH)2D3 administration on intestinal 24-hydroxylase activity. Exogenous administration of 1,25-(OH)2D3, by single bolus injection or constant infusion, increased intestinal 24-hydroxylase activity significantly. Dietary Ca and P restriction both resulted in increased plasma 1,25-(OH)2D3 concentrations several-fold above control rat values (P less than 0.001) and to levels higher than those achieved by constant infusion of 1.3 ng 1,25-(OH)2D3/h. Dietary Ca restriction increased intestinal 24-hydroxylase 6- to 20-fold above that of rats fed a Ca-replete diet (P less than 0.001). Dietary P restriction had no significant effect on intestinal 24-hydroxylase activity. These data suggest that dietary Ca restriction results in increased plasma levels of 1,25-(OH)2D3, which, in turn, leads to up-regulation of intestinal 24-hydroxylase. Conversely, dietary P restriction prevents 1,25-(OH)2D3-mediated up-regulation of 24-hydroxylase.
Reducing cation-anion difference of diets (DCAD) fed just before parturition can prevent milk fever. However this dietary regimen does not entirely eliminate hypocalcemia. Milk fever can also be prevented by exogenous administration of the calcium regulating hormone 1,25-dihydroxyvitamin D. Unfortunately 1,25-dihydroxyvitamin D treatment remains expensive and the pre-partal diets used in most trials would be classified today as high in cations. Solanum glaucophyllum (Sg) is a plant that contains high levels of a glycoside form of 1,25-dihydroxyvitamin D. S. Glaucophyllum is widely distributed in the province of Buenos Aires in Argentina and in Brazil and causes the development of a calcinotic disease in cattle called "Enteque Seco". In order to become active the glycoside must be cleaved to liberate the 1,25(OH) 2 D 3 . Rumen microbes are very efficient at this process. Could administration of Sg leaves to cows that were already being fed a low DCAD pre-partum diet further improve calcium status at calving? Nine multiparous Jersey cows were fed a low DCAD diet prior to calving. Urine pH of cows was maintained below 7.0 in all cows the week prior to parturition. Five cows were daily given 2 or 3 g Sg leaves in gelatin boluses beginning 6 days (on average) before calving and continuing for the first 14 days of lactation. None of the four cows fed the low DCAD diet only developed milk fever. Their blood calcium concentration was 7.6, 7.0 and 8.0 mg/dl the day of calving and d 1 and 2 after calving respectively. Cows receiving Sg in addition to low DCAD diet had significantly higher blood calcium concentration during the periparturient period with blood calcium concentrations of 7.8, 8.8 and 9.3 mg/dl the day of calving and d 1 and 2 after calving respectively. Defining subclinical hypocalcemia as blood calcium <7.5 mg/dl, control cows suffered an average of 3 days of subclinical hypocalcemia and the Sg treated cows suffered 0.8 d of subclinical hypocalcemia the first 2 wk of lactation. Thus, Sg treatment improved calcium status in animals that were also being fed a low DCAD diet. Unfortunately, all cows receiving Sg suffered 1-2 days of hypocalcemia (1 cow developed milk fever) between 6 and 8 days after Sg treatment was ended. Mean blood calcium on d 22 of lactation of Sg cows was 6.9 mg/dl compared with 9.2 mg/dl in untreated cows. It appears that Sg treatment supplanted the cow's own calcium homeostasis mechanisms so that abrupt withdrawal of treatment left the cows temporarily unable to control blood calcium concentration. Additional experiments were conducted using a phased withdraw approach. Three cows were treated with Sg from 5 days prepartum to 7 postpartum (2 g Sg/d) from day 8-14 postpartum (1 g Sg/d) and day 15-21 postpartum (0.5 g Sg/d). The phased withdrawal approach resulted in normal calcium concentration for up to 2 weeks following cessation of Sg. These data suggest that Sg can be used successfully in the prevention of hypocalcemia and that a phased withdrawal approach to removing the exogenous so...
Endometritis and fever are common health disorders that affect dairy cows during the immediate postparturient period and are temporally associated with periparturient immune suppression. The aim of this study was to test the hypothesis that endometritis and fever in dairy cows are associated with suppressed neutrophil functions during the periparturient period.
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