|Carroll, Jeffery - Jeff Carroll|
|Dailey, Jeffery - Jeff|
|Welsh Jr, Tom|
Submitted to: Journal of Animal Science Supplement
Publication Type: Abstract Only
Publication Acceptance Date: 12/15/2008
Publication Date: 2/2/2009
Citation: Ballou, M., Schwertner, L., Carroll, J.A., Hulbert, L.E., Dailey, J.W., Burdick, N., Vann, R., Welsh Jr, T., Randel, R. 2009. Temporal effects on bovine neutrophil function following an intravenous endotoxin challenge [abstract]. Annual meeting of the Southern Section of American Society of Animal Science in Atlanta, GA, on Jan 31 - Feb 4, 2009. Journal of Animal Science. 87(Supplement 2):22. Abstract #65.
Technical Abstract: Neutrophils possess a large array of antimicrobial effector functions. The acute phase response is a complex series of events including a period of inflammation followed by a counter anti-inflammatory state. This study was performed to elucidate any temporal effect of an endotoxin challenge on bovine neutrophil function. Six Brahman bull calves (283 ± 39.9 kg) were fitted with jugular catheters. The next day, all calves were challenged with an intravenous infusion of lipopolysaccharide (LPS; 0.25 micrograms/kg BW). Four hours before and at 0.5, 1.5, 5.5 and 24 hours relative to the LPS challenge, peripheral blood was collected and analyzed to determine the percentage of neutrophils phagocytosing Mannheimia haemolytica and producing an oxidative burst. Since phagocytosis and oxidative burst are dynamic processes we evaluated 2 previously determined incubation times that represented the maximal percentage of neutrophils phagocytosing and producing an oxidative burst as well as the rate to reach that maximum. There was a tendency (P = 0.08) for an interaction between time following the LPS challenge and incubation time for the percentage of neutrophils phagocytosing. Both the rate and maximal percentage of neutrophils increased following the LPS challenge peaking at 1.5 hours; however, at 5.5 hours after the challenge, the maximal neutrophils phagocytosing had returned to baseline levels; whereas the rate did not completely return to baseline levels until 24 hours following the LPS challenge. Similarly, there was an interaction (P < 0.01) between time following LPS and incubation time for the percentage of neutrophils producing an oxidative burst. The rate increased within 0.5 hours (P < 0.05), plateaued at 1.5 hours, and remained elevated at 24 hours; whereas the maximal percentage of neutrophils producing an oxidative burst was not elevated until 24 hours (P < 0.01). These data indicate that that the acute phase response to LPS increases the percentage of neutrophils phagocytosing Mannheimia haemolytica and producing an oxidative burst. Furthermore, the rate to reach the maximum rather than the maximal percentage of neutrophils is more responsive to the effects of LPS.