|Cheng, Heng Wei|
Submitted to: ARS Immunology Workshop
Publication Type: Abstract Only
Publication Acceptance Date: 5/6/2003
Publication Date: 5/6/2003
Citation: EICHER, S.D., CHENG, H. TOLL-LIKE RECEPTOR AND ACUTE PHASE CYTOKINE EXPRESSION IN GENETICALLY SELECTED LINE OF LAYERS FOLLOWING AN LPS CHALLENGE. ARS IMMUNOLOGY WORKSHOP. 2003. V. 17:C51.
Technical Abstract: A multi-disciplinary approach is essential to ascertain the well-being of farm animals. The Livestock Behavior Research Unit uses behavioral, physiological, and immunological measures to answer well-being questions for poultry, swine, and dairy cattle. The innate immune system is frequently the first immune responder during many stressors and the resulting acute phase cytokines affect behavior and learning. Toll-like receptors are the pathogen recognition molecules that initiate the cascade that increases the acute phase cytokines. The effect of pathogens and stressors on the toll-like receptors of farm animals is not known. A study has been completed that examines the effect of lipopolysaccharide (LPS) on RNA toll-like receptor expression in chickens. The objective of this study was to determine expression of TLR2, TLR4, and two acute phase cytokines (interleukin-1 and tumor necrosis factor-alpha) following an LPS challenge of two genetic lines of layers divergently selected for aggression (aggressive, MBB and passive, KGB)and one commercial genetic line (COMM). The 3 lines of layers were given LPS (5.0 mg/kg of body weight), then organs (heart, liver, and spleen) were weighed and lung, liver, and spleen tissues were collected at 0, 24, and 72 hours following a single LPS i.v. injection. RNA was extracted from the tissues and subjected to real-time RT-PCR. Heart and spleen weights had genetic line (P < 0.01) and time effects (P < 0.05 and 0.01, for heart and spleen respectively). Liver weights were different for genetic line (P < 0.01) but not time. Liver IL-1 and TLR2 had time effects (P < 0.01) but were not different among treatments. Liver TNF and TLR4 were not different over time or among treatments. Lung IL-1, TLR2, TLR4, and TNF were different over time (P < 0.05 for TLR4 and P < 0.01 for IL-1, TLR2, and TNF) but not among treatments. Spleen IL-1, TLR2, TLR4, and TNF were different over time but not among treatments (P < 0.05 for IL-1, P < 0.01 for TLR2, TLR4, and TNF). No treatment by time interactions were detected for any of these variables (P > 0.05). The only effects of genetic line were liver and spleen weight. Toll-like receptors 2 and 4 and cytokine changes were not influenced by genetic lines, only by time. Toll-like receptor expression was dissimilar for the two receptors that we investigated. Toll-like receptor 2 had effects of time in all three tissues, while TLR4 was influenced by time only in lung and spleen. Toll-like receptor 2 increased expression in the liver and spleen by 24 hours, but did not increase in the lung until 72 hours post-LPS injection. Liver TLR2 remained elevated through the 72 hour sample. Therefore, this genetic selection did not alter RNA expression of these innate immune receptors and cytokines. Since toll-like receptors recognize heat-shock proteins, further exploration of toll-like receptor expression during heat stress in chickens is in progress.