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Title: MECHANISM OF ENDOTOXIN PRIMING ON PHAGOCYTOSIS AND OXIDATIVE BURST ACTIVITYIN BOVINE NEUTROPHILS

Author
item DOSOGNE, H - UNIVERSITY OF GHENT
item BURVENICH, C - UNIVERSITY OF GHENT
item DIAZ-FRAILE, A - UNIVERSITY OF GHENT
item MASSART-LE'N, A - UNIVERSITY OF GHENT
item Paape, Max

Submitted to: Belgium Society for Fundamental and Clinical Physiology and Pharmacology
Publication Type: Proceedings
Publication Acceptance Date: 8/1/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: The objectives of the present study were 1) to compare the response to LPS between PMN from the blood of early and mid-lactation dairy cows and 2) to evaluate the role of TNF-a in the response. Blood from 5 early and 5 mid-lactation cows was collected. PMN in whole blood were incubated with different concentrations of LPS: 0; 0.1; 1; 10; 100 and 10.000 ng/ml. Priming of all PMN functions was maximal at 1 ng/ml LPS and there was never an inhibition of PMN functions compared to control values. PMN oxidative burst activity without LPS stimulation was higher in mid-lactation cows than in early lactation cows but there was no difference between the 2 groups of cows in phagocytosis. The stimulation of oxidative burst activity of PMN from early lactation cows by LPS was stronger than in mid-lactation cows. To investigate the TNF-a-dependence of the LPS response, PMN were first incubated with several dilutions of anti-bovine TNF-a and then stimulated with LPS. A dilution of 1/100 of the antibody appeared to be necessary to inhibit the LPS stimulation, but the effect of LPS never seemed to be blocked completely at any LPS concentration. In conclusion, PMN oxidative burst was decreased in early lactation cows and the response to LPS was more pronounced in comparison with mid-lactation cows. TNF-a was at least partially responsible for the priming of PMN by LPS, suggesting a role for this cytokine in the pathology of endotoxin-related diseases.