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Intramammary Glucocorticoid During a Mammary Immune Response to Lipopolysaccharide Modulates the Blood-Milk Barrier
Glucocorticoids such as prednisolone are frequently used in addition to intramammary antibiotic therapy to increase the cure rate of mastitis in dairy cows. This study aimed to investigate the effects of intramammary administered prednisolone during the mammary immune response to lipopolysaccharide (LPS).
Five healthy mid-lactation Holstein dairy cows received one of four intramammary treatments in each of their four quarters: prednisolone (10 mg), LPS (100 μg), LPS (100 μg) and prednisolone (10 mg), or saline control. Milk samples were taken 0, 3, 6, 9, 12, 24, and 36 hours after challenge. Somatic cell count (SCC), and concentrations of lactate dehydrogenase (LDH), serum albumin (SA), and tumor necrosis factor-alpha (TNFα) in milk and mRNA abundance of TNFα, Interleukin (IL)-8, and IL-1β in milk somatic cells were compared at each timepoint. Differences between quarters were tested by analysis of variance using a MIXED procedure and were considered significant if P<0.05.
Control and prednisolone infused quarters did not show changes of SCC, LDH, SA, and TNFα concentrations in milk and mRNA expression of TNFα, IL-1β, and IL-8 in milk somatic cells. Concentrations of SCC and TNFα in milk increased similarly in LPS challenged quarters independent of additional prednisolone application. However, the increase of LDH activity and SA concentration in LPS challenged quarters was diminished by prednisolone (P=0.028 and P<0.001, respectively) from 1352±845 to 264±107 U/L for LDH, and 8.17±0.29 to 2.68±0.30 mg/L for SA at 6 h after challenge, respectively. The mRNA abundance of TNFα, IL-8, and IL-1β in milk somatic cells increased in response to LPS challenge unaffected by prednisolone.
In conclusion, the intramammary administration of the glucocorticoid prednisolone does not induce an increase of SCC, changes in concentrations of blood components in milk, and does not change the production of TNFα, IL-8, and IL-1β in milk cells in response to intramammary LPS challenge. However, the intramammary administration of prednisolone clearly reduces the disruption of the blood-milk barrier induced by endotoxin challenge shown by a reduced appearance of blood constituents like SA or LDH in milk. This effect could have an important influence on the severity and on the cure rate of mastitis.
Keywords: prednisolone, blood-milk barrier, mastitis