|Tan, J -|
|Guo, Y -|
|Applegate, Todd -|
Submitted to: Poultry Science Association Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: April 1, 2013
Publication Date: July 22, 2013
Citation: Tan, J.Z., Guo, Y.M., Eicher, S.D., Applegate, T.J. 2013. Dietary L-arginine supplementation modulates lipopolysaccharide-induced systemic inflammatory response in broiler chickens. Poultry Science Association Meeting Abstract. 92(E-suppl.1):. Technical Abstract: This study was conducted to evaluate whether dietary supplementation with L-arginine (Arg) could attenuate lipopolysaccharide (LPS)-induced systemic inflammatory response through LPS/TLR-4 signaling pathway in broilers. The experiment was designed as a 2 × 3 factorial arrangement (n = 8 cages/treatment; 6 birds/cage) with 3 dietary Arg concentrations (1.05, 1.42, and 1.90%) and 2 immune treatments (i.p. injection of lipopolysaccharide (LPS) or saline). From 14 to 21 d of age, LPS (Escherichia coli 0111:B4) was injected 4 times at 48-h intervals (1 mg/kg of BW), after which spleen and cecal tonsil samples were obtained. The LPS injection significantly decreased BW gain and feed intake (FI), increased feed conversion ratio (FCR) from 14 to 21 d of age (P<0.05). LPS injection increased (P<0.05) mRNA expression of pro-inflammation cytokines IL-1ß and IL-6 in the spleen and cecal tonsils, and the dietary Arg supplementation decreased (P<0.05) the expression of IL-1ß in the spleen and cecal tonsils. The only cytokine that had a significant Arg*LPS interaction was Il-1ß in the cecal tonsils, with increasing dietary Arg reducing expression in LPS challenged birds (P<0.005). LPS injection increased TLR-4 (P<0.05) in the spleen and celcal tonsils, dietary Arg supplementation decreased (P<0.05) the TLR-4 expression in spleen and cecal tonsils, which likely induced the measured decrease (P<0.05) of NFkappaB expression in the cecal tonsils. Thus, results suggest that dietary Arg supplementation modulates the inflammatory response partly through the suppression of LPS/TLR-4 pathway.