Supplemental dietary L-arginine attenuates intestinal mucosal disruption during a coccidial vaccine challenge in broiler chickens.

Abstract

The present study investigated the effects of dietary arginine (Arg) supplementation on intestinal structure and functionality in broiler chickens subjected to coccidial challenge. The present study was a randomised complete block design employing a 3×2 factorial arrangement (n 8) with three dietary concentrations of Arg (11·1, 13·3 and 20·2g/kg) with or without coccidial vaccine challenge (unchallenged and coccidial challenge). On day 14, birds were orally administered with coccidial vaccine or saline. On day 21, birds were killed to obtain jejunal tissue and mucosal samples for histological, gene expression and mucosal immunity measurements. Within 7d of the challenge, there was a decrease in body-weight gain and feed intake, and an increase in the feed:gain ratio (P<0·05). Jejunal inflammation was evidenced by villus damage, crypt dilation and goblet cell depletion. Coccidial challenge increased mucosal secretory IgA concentration and inflammatory gene (iNOS, IL-1β, IL-8 and MyD88) mRNA expression levels (P<0·05), as well as reduced jejunal Mucin-2, IgA and IL-1RI mRNA expression levels (P<0·05). Increasing Arg concentration (1) increased jejunal villus height (P<0·05) and linearly increased jejunal crypt depth (P<0·05); (2) quadratically increased mucosal maltase activity (P<0·05) and linearly decreased mucosal secretory IgG concentration (P<0·05) within the coccidiosis-challenged groups; and (3) linearly decreased jejunal Toll-like receptor 4 (TLR4) mRNA expression level (P<0·05) within the coccidiosis-challenged groups. The mRNA expression of mechanistic target of rapamycin (mTOR) complex 1 pathway genes (mTOR and RPS6KB1) and the anti-apoptosis gene Bcl-2 quadratically responded to increasing dietary Arg supplementation (P<0·05). These results indicate that dietary Arg supplementation attenuates intestinal mucosal disruption in coccidiosis-challenged chickens probably through suppressing TLR4 and activating mTOR complex 1 pathways.