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Title: IN VITRO REGULATION OF MAC-1 EXPRESSION ON BOVINE POLYMORPHONUCLEAR LEUKOCYTES BY ENDOTOXIN AND TUMOR NECROSIS FACTOR-ALPHA AT DIFFERENT STAGES OF LACTATION

Author
item DIEZ-FRAILE, ARACELI - GHENT UNIVERSITY BELGIUM
item MEYER, EVELYNE - GHENT UNIVERSITY BELGIUM
item DUCHATEAU, LUC - GHENT UNIVERSITY BELGIUM
item Paape, Max
item BURVENICH, CHRISTIAN - GHENT UNIVERSITY BELGIUM

Submitted to: Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2004
Publication Date: 7/1/2004
Citation: Diez-Fraile, A., Meyer, E., Duchateau, L., Paape, M.J., Burvenich, C. 2004. In vitro regulation of mac-1 expression on bovine polymorphonuclear leukocytes by endotoxin and tumor necrosis factor-alpha at different stages of lactation. Veterinary Research. 68(3):232-235.

Interpretive Summary: Bacterial invasion and growth within the mammary gland is the main cause of mastitis. Invading bacteria settle next to the epithelial cells lining the mammary ducts, absorbing nutrients from milk while expelling harmful toxins that attack and destroy the epithelium. White blood cells called macrophages have cell surface molecules called CD14. When these molecules are stimulated by bacterial toxins, they release chemicals that cause recruitment of another type of white blood cell called neutrophils to the infection site. Neutrophils specialize in eating and destroying bacteria. The sooner the neutrophils arrive at the infection site the sooner the infection will be contained and eliminated. Scientists have discovered that the CD14 molecules are not very abundant on macrophages during early lactation when compared to later lactation. Dairy cows are at a higher risk of getting mastitis during early lactation, soon after calving. This discovery could lead to ways of getting neutrophils to the site of infection faster to eliminate invading mastitis pathogens.

Technical Abstract: This study intends to clarify some of the underlying mechanisms leading to the increased susceptibility of dairy cows to periparturient diseases, such as coliform mastitis. Surface expression of the adhesion molecule Mac-1 (CD11b, CR3) on PMN and of CD14 on monocytes was measured in early (EL), peak (PL), and mid lactation (ML) by flow cytometric analysis. In addition, we evaluated the ex vivo effect of lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-alpha on CD11b surface density of PMN at different stages of lactation. The basal expression of CD11b on PMN was not significantly altered during EL when compared with PL or ML, while resting monocytes expressed diminished levels of CD14 at EL. Both LPS and TNF-alpha acted as direct stimulants of CD11b density on PMN. The relative increase of CD11b on PMN after incubation with LPS or TNF-alpha did not significantly differ among EL, PL, or ML at any of the concentrations tested. Hence, it seems that decreased levels of CD14 on circulating monocytes detected during EL do not account for an altered stimulus-specific activation of CD11b surface density on blood PMN. LPS-induced ex vivo upregulation of CD11b on PMN could partially be abrogated by anti-bovine TNF-alphaMAb.