and protective effect of arginine against intestinal inflammatory response induced by in broiler chickens.

BACKGROUND

Necrotic enteritis is a widespread disease in poultry caused by We previously reported that dietary arginine supplementation protected the intestinal mucosa of broiler chickens with necrotic enteritis, but the related protective mechanisms remain unclear. The trial was designed as a 2 × 2 factorial arrangement to evaluated the effects of arginine supplementation on inflammatory responses, arginine transporters, arginine catabolism and JAK-STAT signalling pathway in broiler chickens challenged with or without . Furthermore, we validated the results using intestinal epithelial cells of chicken embryos.

RESULTS

infection markedly increased gut gross pathological and histopathological lesion scores, promoted liver invasion, reduced serum arginine levels, and elevated jejunal mucosal lysozyme activities ( < 0.05), but these effects were significantly reversed by arginine supplementation ( < 0.05). The challenge significantly increased serum procalcitonin levels, jejunal mucosal iNOS activities and jejunal , , cationic amino acid transporter (), and mRNA expression ( < 0.05), whereas arginine supplementation significantly reduced jejunal , , , , , and mRNA expression ( < 0.05). Arginine supplementation significantly attenuated the challenge-induced increases in jejunal , arginase 2, arginine decarboxylase, arginine:glycine amidinotransferase, , , , and mRNA expression ( < 0.05). The experiment showed that challenge markedly increased cellular cytotoxicity and the mRNA expression of , , , and ( < 0.05), which were significantly reversed by 50 μmol/L and/or 400 μmol/L arginine pre-treatment ( < 0.05).

CONCLUSIONS

Arginine prevented challenge-induced circulated arginine deficiency, normalized intestinal arginine transport and catabolism, down-regulated JAK-STAT signalling pathway and attenuated the inflammatory response, which exerted protective effects on the intestine of broiler chickens.