title: Differential glucocorticoid-induced closure of the blood-milk barrier during lipopolysaccharide- and lipoteichoic acid-induced mastitis in dairy cows.
abstract: Bacteria invading the mammary gland can cause pathogen-dependent differences in the permeability of the blood-milk barrier leading to the differential paracellular transfer of blood and milk components. Glucocorticoids such as prednisolone (PRED) are known to increase the integrity of the blood-milk barrier and quickly restore the decreased milk quality associated with mastitis. The objective of this study was to examine the effect of intramammary PRED on the differential permeability of the blood-milk barrier during mastitis induced by lipopolysaccharide (LPS) from Escherichia coli or lipoteichoic acid (LTA) from Staphylococcus aureus. Thirty-one dairy cows, divided into 6 groups, were injected via a teat canal with LPS, LTA, LPS and PRED, LTA and PRED, saline (control), or PRED. Milk and blood samples were collected 0 to 8h after challenge and analyzed for somatic cell count, IgG, serum albumin, and lactate dehydrogenase in milk, or α-lactalbumin in plasma. Somatic cell count was similarly elevated in LPS- and LTA-challenged quarters and was reduced to control quarter levels only in LTA-challenged quarters with PRED administration. Lactate dehydrogenase activity was highly elevated in LPS quarters and only slightly elevated in LTA quarters, but decreased to control quarter levels with PRED administration. For serum albumin and IgG, only LPS quarters showed an elevation in concentration and PRED treatment reduced the concentration to control quarter level. We found no differences in α-lactalbumin concentrations in plasma in PRED-treated cows compared with cows that only received 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 that, in turn, can be manipulated by intramammary glucocorticoids. The results show that the administration of PRED during mastitis increases the blood-milk barrier integrity but has implications in reducing the transfer of IgG that specifically occurs during E. coli mastitis. In addition, it can also reduce the number of migrating immune cells dependent on the mastitis-inducing pathogen. Potential effects of PRED on the cure of naturally occurring mastitis have to be taken into consideration.
authors.affiliation: Veterinary Physiology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland; Graduate School for Cellular and Biomedical Science, University of Bern, 3012 Bern, Switzerland.
authors.forename: Samantha K
authors.initials: SK
authors.lastname: Wall
authors.affiliation: Veterinary Physiology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland.
authors.forename: Lorenzo E
authors.initials: LE
authors.lastname: Hernández-Castellano
authors.affiliation: Veterinary Physiology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland.
authors.forename: Amir
authors.initials: A
authors.lastname: Ahmadpour
authors.affiliation: Veterinary Physiology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland.
authors.forename: Rupert M
authors.initials: RM
authors.lastname: Bruckmaier
authors.affiliation: Veterinary Physiology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland. Electronic address: olga.wellnitz@vetsuisse.unibe.ch.
authors.forename: Olga
authors.initials: O
authors.lastname: Wellnitz
mesh_terms: D000818:Animals; D002417:Cattle; D004926:Escherichia coli / Q000502:physiology; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000382:microbiology / Q000503:physiopathology / Q000662:veterinary*; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008321:Mammary Glands, Animal / Q000382:microbiology / Q000503:physiopathology*; D008414:Mastitis, Bovine / Q000188:drug therapy* / Q000382:microbiology / Q000503:physiopathology; D011239:Prednisolone / Q000494:pharmacology*; D011897:Random Allocation; D013203:Staphylococcal Infections / Q000382:microbiology / Q000503:physiopathology / Q000662:veterinary*; D013211:Staphylococcus aureus / Q000502:physiology; D013682:Teichoic Acids / Q000494:pharmacology
chemical_list: D005938:Glucocorticoids; D008070:Lipopolysaccharides; D013682:Teichoic Acids; C009900:lipoteichoic acid; D011239:Prednisolone
keywords: blood-milk barrier; endotoxin; glucocorticoid; mastitis