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Title:   Author  item
                                            Carroll, Jeffery

                                                         - *Jeff Carroll*item
                                            Hulbert, Lindseyitem
                                            BURDICK, NICOLE - TEXAS AGRILIFE RESEARCHitem
                                            CALDWELL, LISA - TEXAS AGRILIFE RESEARCHitem
                                            BALLOU, MIKE - TEXAS TECH UNIVERSITYitem
                                            ARTHINGTON, JOHN - UNIVERSITY OF FLORIDAitem
                                            VANN, RHONDA - TEXAS AGRILIFE RESEARCHitem
                                            LOYD, ANDREA - TEXAS AGRILIFE RESEARCHitem
                                            WELSH JR, TOM - TEXAS AGRILIFE RESEARCHitem
                                            RANDEL, RON - TEXAS AGRILIFE RESEARCH
  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: 10/16/2009
                                    Citation: Carroll, J.A., Hulbert, L.E., Burdick, N., Caldwell, L., Ballou, M., Arthington, J., Vann, R., Loyd, A., Welsh Jr, T., Randel, R. 2009. The acute phase response: Differentiating corticotrophin-releasing hormone (CRH)- versus lipopolysaccharide (LPS)-induced proinflammatory cytokine and acute phase protein profiles in beef calves [abstract]. Annual meeting of the American Dairy Science Association, July 12-16, 2009, Montreal, Canada. Journal of Animal Science 87(E-Supplement 2):702.Interpretive Summary:
                                Technical Abstract: Development of methods to effectively attenuate potentially detrimental effects of various stressors encountered by livestock depends on understanding unique stressor-specific responses. The objective of this study was to profile indicators of the acute phase immune response to compare and contrast potential differences between CRH- and LPS-induced stress responses. Purebred Brahman bull calves (n = 11; 226.9±12.6 kg) were transported 770 km from Overton, TX, to Lubbock, TX, and fitted with indwelling jugular catheters after 24 h of rest. Twenty-four h afterwards, blood samples were collected at 30-min intervals from -2 to 8 h, and again at 12 and 24 h, relative to an i.v. infusion of either LPS (0.25 micrograms/kg BW) or CRH (0.5 micrograms/kg BW) at 0 h. Serum was stored at -80°C until analyzed for tumor necrosis factor-alpha (TNF), interleukin 6 (IL-6), interferon gamma (IFN) and haptogolobin (Hp). Compared to pre-challenge concentrations, CRH induced a single peak in serum TNF starting at 2.5 h (P less than or equal to 0.01) and lasting until 4 h (P less than or equal to 0.07), whereas LPS induced a biphasic response beginning at .5 h (P less than or equal to 0.04) with peaks at 1.5 and 3.5 h, and lasting until 7.5 h (P less than or equal to 0.01). For IL-6, CRH induced a single peak beginning at 3 h (P less than or equal to 0.01) and only lasting for .5 h. In contrast, LPS induced a biphasic IL-6 response beginning at 1.5 h (P less than or equal to 0.01), peaking at 2.5 h and 6 h, and lasting until 12 h (P less than or equal to 0.03). For IFN, CRH induced a single peak at 3 h (P less than or equal to 0.01), beginning at 2.5 h (P less than or equal to 0.07) and lasting until 3.5 h (P less than or equal to 0.01). LPS induced a multiphasic IFN response beginning at .5 h (P less than or equal to 0.01) and lasting until 24 h (P less than or equal to 0.01) with peaks at 2.5, 3.5, and 6 h. For Hp, CRH-induced a single spike at 4 h (P less than or equal to 0.02) that had ended by 6 h (P greater than or equal to 0.14) whereas LPS induced Hp concentrations continued to escalate even at the 24 h time period (P less than or equal to 0.01). These data demonstrate that the stress response in beef calves, either simulated by CRH or induced by endotoxin, is comprised of specific immunological profiles that may be as unique as the stressor itself.


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