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867
Intramammary prednisolone affects the permeability of the blood-milk barrier during LPS and LTA induced mastitis in dairy cows

Saturday, July 23, 2016: 11:30 AM
155 B (Salt Palace Convention Center)
Samantha K Wall , Veterinary Physiology, Vetsuisse Faculty University of Bern, Bern, Switzerland
Lorenzo E Hernandez-Castellano , Veterinary Physiology, Vetsuisse Faculty University of Bern, Bern, Switzerland
Rupert M Bruckmaier , Veterinary Physiology, Vetsuisse Faculty University of Bern, Bern, Switzerland
Olga Wellnitz , Veterinary Physiology, Vetsuisse Faculty University of Bern, Bern, Switzerland
Abstract Text:

Mastitis can induce pathogen dependent changes in the permeability of the blood-milk barrier and therefore the paracellular transfer of blood and milk components. Glucocorticoids are known to increase the integrity of this barrier. The objective of this study was to examine the effect of intramammary prednisolone (PRED) on the blood-milk barrier in cows during mastitis induced by lipopolysaccharide (LPS) from Escherichia coli or by lipoteichoic acid (LTA) from Staphylococcus aureus. Thirty-one dairy cows, divided into 6 groups, were intramammarily challenged in one quarter with LPS, LTA, LPS and PRED, LTA and PRED, saline (control), or PRED. Quarters had a somatic cell count (SCC) of 60 ± 10 x 103 cells/mL before the experiment. The chosen doses of LPS and LTA induced a similar increase of SCC to 1420 ± 360 x 103cells/mL at 4 h after challenge. Milk and blood samples were collected hourly from 0 to 8 h after challenge. Milk was analyzed for SCC, immunoglobulin (Ig) G, serum albumin (SA), and lactate dehydrogenase (LDH). Plasma was tested for the milk protein alpha-lactalbumin (ALA).  Differences between treatments were tested by analysis of variance using a MIXED procedure and were considered significant if P < 0.05. The SCC in milk of control quarters and quarters treated only with PRED did not change throughout the experiment. In LTA challenged quarters with additional PRED administration, there was a reduction in SCC to control quarter level, whereas in LPS treated quarters, additional PRED administration had no effect on SCC. LDH activity did not significantly increase in LTA treated quarters, but increased in LPS quarters from 27±7 U/L before challenge to 404 ± 115 U/L at 6 h after challenge, and decreased to control quarter levels with additional PRED administration. For SA and IgG, only LPS quarters showed an elevation from 0.25 ± 0.07 and 0.32 ± 0.04 mg/mL to 1.34 ± 0.57 and 1.16 ± 0.52 mg/mL, respectively, at 4 h after challenge. The PRED treatment reduced both concentrations to control quarter levels. There were no differences in plasma ALA concentrations in PRED treated cows compared to cows that received only LPS or LTA. In conclusion, the pathogen specific appearance of blood constituents in milk during mastitis demonstrates a differential activation of the blood-milk barrier. These differential effects can be influenced by intramammary administration of glucocorticoids in a pathogen specific manner.

Keywords: blood-milk barrier, endotoxin, glucocorticoid, mastitis