|Carroll, Jeffery - Jeff Carroll|
|Welsh Jr, Tom|
Submitted to: Joint Abstracts of the American Dairy Science and Society of Animal Science
Publication Type: Abstract Only
Publication Acceptance Date: 3/18/2009
Publication Date: 11/18/2009
Citation: Ballou, M., Hulbert, L.E., Schwertner, L., Carroll, J.A., Caldwell, L., Vann, R., Welsh Jr, T., Randel, R. 2009. Influence of an in vivo corticotropin-releasing hormone (CRH) challenge on ex vivo phagocytic and oxidative burst capacities of bovine neutrophils [abstract]. Annual meeting of the American Dairy Science Association, July 12-16, 2009, Montreal, Canada. Journal of Animal Science 87(E-Supplement 2):194. Interpretive Summary:
Technical Abstract: Various stressors are linked in the etiology of disease states. The adverse actions of pathogens are limited by the ability of neutrophils to phagocytize and neutralize them. The objective of this study was to elucidate the temporal effects of an exogenous CRH challenge on neutrophil function. Brahman heifers (193.2±9.4 kg; n=6) were challenged with an intravenous bolus of bCRH (0.5 micrograms/kg BW). Immediately before (baseline) and at 1, 2, 4, 6, and 24 h relative to the challenge, peripheral blood samples were collected to analyze phagocytic and oxidative burst capacities of neutrophils following 15-min or 60-min incubation periods with pre-opsonized Mannheimia haemolytica. Data are presented as the percentage and mean fluorescence intensity (MFI) of neutrophils phagocytizing or undergoing an oxidative burst. In addition, overall indices of phagocytosis and oxidative burst capacities were calculated as the percentage of neutrophils multiplied by their respective MFI. The percentage of neutrophils phagocytizing at the 15-min incubation was rapidly suppressed following the CRH challenge, but within 24 h values were not different from baseline. Neutrophils incubated for 60-min were initially suppressed, but compensated with more phagocytizing neutrophils 2 h after the challenge and within 4 h there was no difference relative to baseline. Mean fluorescence intensities of phagocytizing neutrophils were less responsive to the CRH challenge. The percentage of neutrophils producing an oxidative burst was suppressed at the 15-min incubation reaching the nadir at 2 h and returning to baseline at 6 h after the challenge. However, the MFI and the oxidative burst capacity index of neutrophils producing an oxidative burst for both incubation times decreased rapidly and remained suppressed 24 h after the challenge. These data indicate that both phagocytosis and oxidative burst capacities of neutrophils are suppressed by an in vivo administration of CRH. Diminished neutrophil capacities concurrent with or subsequent to a stressful event may contribute to increased susceptibility to pathogens.