Immune responses to dietary beta-glucan in broiler chicks during an Eimeria challenge

Escalating consumer concerns regarding pathogen resistance have placed the poultry industry under mounting pressure to eliminate the use of chemotherapeutic agents as feed additives. One possible alternative receiving increased attention is the use of immunomodulators such as β-glucan. A study was conducted to investigate the effects of a yeast-derived β-glucan (Auxoferm YGT) on broiler chick performance, lesion scores, and immune-related gene expression during a mixed Eimeria infection. Day-old chicks were fed diets containing 0, 0.02, or 0.1% YGT. On d 8 posthatch, one-half of the replicate pens were challenged with a mixed inoculum of Eimeria acervulina, Eimeria maxima, and Eimeria tenella. Measurements were taken and samples collected on d 4, 10, 14, and 21 posthatch. Dietary supplementation had no effect on performance or mortality. On d 14, 3 birds per pen (n = 24/treatment) were scored for intestinal coccidia lesions. Gross lesion severity was significantly reduced in birds supplemented with 0.1% YGT. On d 10, inducible nitric oxide synthase (iNOS) expression was downregulated in the jejunum of challenged birds fed 0.1% YGT. Expression of iNOS in the ileum was downregulated in the nonchallenged birds, but upregulated in the challenged birds fed 0.1% YGT on d 14. Interleukin (IL)-18 was upregulated in the jejunum of 0.1% YGT-treated birds. Interferon (IFN)-γ expression was decreased in challenged and nonchallenged birds fed 0.1% YGT. The IL-4 expression was downregulated in the nonchallenged birds with 0.1% YGT diet supplementation. The IL-13 and mucin-1 levels were also reduced due to β-glucan supplementation. Mucin-2 expression was increased in the nonchallenged birds, but decreased in the infected birds fed 0.1% YGT. These results suggest that although Auxoferm YGT at doses of 0.02 and 0.1% does not influence performance, it significantly reduces lesion severity and is capable of altering immune-related gene expression profiles, favoring an enhanced T helper type-1 cell response during coccidiosis.