ENHANCING ANIMAL WELL-BEING, IMMUNOCOMPETENCE, AND PERFORMANCE IN SWINE AND BEEF CATTLE
Location: Livestock Issues Research
Title: Acute modulation of cytokine gene expression in bovine PBMCs by endogenous cortisol
Submitted to: American Society of Animal Science Southern Section Meeting
Publication Type: Abstract Only
Publication Acceptance Date: November 3, 2010
Publication Date: August 11, 2011
Citation: Burdick, N.C., Agado, B.J., Randel, R.D., Neuendorff, D.A., Carroll, J.A., Vann, R.C., Chitko-McKown, C.G., Lawhon, S.D., Welsh Jr, T.H. 2011. Acute modulation of cytokine gene expression in bovine PBMCs by endogenous cortisol [abstract]. Journal of Animal Science. 89:A124(E-Suppl. 2).
Cortisol suppresses many aspects of immune function. However, recent publications suggest acute cortisol exposure may actually enhance immune function (Dhabhar, Neuroimmunomod 2009;16:300). The objective of this study was to determine the influence of acute increases in endogenous cortisol on expression of cytokines and associated receptors in isolated peripheral blood mononuclear cells (PBMCs). Brahman heifers (n=12; 334±12 kg BW) had jugular catheters inserted prior to a challenge with 0.1 IU/kg BW ACTH. Blood samples were collected into EDTA vacutainers at 0, 1, 2, and 4 hr relative to the challenge. Plasma cortisol was determined by RIA. The PBMCs were isolated via density gradient centrifugation and frozen at -80 deg C until RNA isolation. Extracted RNA was amplified by real-time RT-PCR to determine expression of 11-beta Hydroxysteroid dehydrogenase I (11-betaHSD I), 11-betaHSD II, ACTH Receptor (ACTHR) Interleukin-1beta (IL-1beta), IL-2, IL-6, IL-1 Receptor (IL-1R), and Tumor Necrosis Factor-alpha Receptor (TNF-alphaR). Cytokine expression data are expressed as the fold change in gene expression relative to samples collected at time 0. All data were analyzed using the mixed procedure of SAS, with time and animal as class and random variables, respectively. Expression of 11-betaHSD I, 11-betaHSD II, IL-1R, TNF-alphaR increased and were greatest at 4 hr (5.4 ± 1.1 fold, 1.8 ± 0.2 fold, 28.8 ± 7.6 fold, and 2.9 ± 0.5 fold, respectively; P = 0.05). However, the 4-hr samples were the last samples collected and therefore, it is not clear whether expression of these genes continued to increase. Expression of the ACTHR (P = 0.31), IL-1beta (P = 0.34), IL-2 (P = 0.30), and IL-6 (P = 0.14) did not change. This suggests that stimuli that increase endogenous cortisol concentrations may influence the expression of cytokines, and therefore modulate or possibly prime the immune system prior to a subsequent immune challenge.