ENHANCING ANIMAL WELL-BEING, IMMUNOCOMPETENCE, AND PERFORMANCE IN SWINE AND BEEF CATTLE
Location: Livestock Issues Research
Title: Influence of an in vivo endotoxin challenge on ex vivo phagocytic and oxidative burst capacities of bovine neutrophils
| Ballou, Mike - TEXAS TECH UNIVERSITY |
| Hulbert, Lindsey |
| Schwertner, Luke - TEXAS TECH UNIVERSITY |
| Caldwell, Lisa - TEXAS AGRILIFE RESEARCH |
| Vann, Rhonda - MISSISSIPPI STATE UNIV |
| Welsh Jr, Tom - TEXAS AGRILIFE RESEARCH |
| Randel, Ron - TEXAS AGRILIFE |
Submitted to: Joint Abstracts of the American Dairy Science and Society of Animal Science
Publication Type: Abstract Only
Publication Acceptance Date: March 18, 2009
Publication Date: September 6, 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 endotoxin 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):#193.
Neutrophils promote health by reducing the early growth of invading pathogens. The objective of this study was to elucidate the temporal effects of an exogenous endotoxin (lipopolysaccharide; LPS) challenge on neutrophil function. Brahman heifers (186.1±11.8 kg; n=6) were challenged with an intravenous bolus of LPS (0.25 micrograms/kg BW). Immediately before (baseline) and at 1, 2, 4, 6, and 24 h relative to 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 as well as the MFI of phagocytizing neutrophils increased following the LPS challenge. Therefore, the phagocytic index increased, peaking at 1 and 2 h for the 15- and 60-min incubations, respectively. Within 24 h, the phagocytic index returned to baseline for the 15-min incubation, but there was a tendency (P < 0.06) for the phagocytic index to remain elevated for the 60-min incubation, reflecting an increased percentage of phagoycytizing neutrophils. The percentage of neutrophils producing an oxidative burst increased, but only in the neutrophils incubated for 15 min. The MFI of the neutrophils producing an oxidative burst decreased rapidly for both incubation times and remained suppressed 24 h after the challenge. These data indicate that an LPS challenge stimulates the phagocytic capacity of neutrophils. However, despite more “early-responding” neutrophils undergoing an oxidative burst, the MFI and overall oxidative burst index are suppressed and remain so 24 h following an LPS challenge. The suppressed oxidative burst capacity may compromise the ability of neutrophils to control the growth of pathogens; alternatively, it may be a compensatory mechanism limiting excessive pathology.