Immunology and Pathology: Poultry Immunology and Pathology

Abstract

Immunomodulators like β-glucans have attracted considerable attention as potential alternatives to the prophylactic use of antibiotics. Despite increasing research, little is known about their regulatory influence on immune function in poultry. Two studies were conducted to evaluate the effects of a yeast-derived β-glucan (Auxoferm YGT) on gene expression of T helper cytokines in the intestine. Day old chicks were fed a diet containing 0, 0.02, or 0.1% β-glucan. For the first study, small intestinal sections were collected on d 7 and d 14 to evaluate gene expression by quantitative real-time PCR. On d 7, interleukin (IL)-18 expression was upregulated in the jejunum but decreased on d 14 in the duodenum of the 0.02% β-glucan birds. Expression of IL-18 also decreased on d14 in the ileum of both β-glucan groups when compared with control. On d 7, IL-4 expression was downregulated in both β-glucan treated groups in the duodenum and in the 0.1% treated group in the jejunum and ileum. In contrast, IL-4 was upregulated in the duodenum of treated birds and in the ileum of 0.1% fed birds on d 14. Similarly, IL-13 was downregulated in all intestinal sections of 0.1% β-glucan fed birds on d 7. The second study included a mixed Eimeria infection on d 8 and samples were collected on d 10, 14, and 21 post-hatch. Despite the fact that no significant differences were seen among treatment groups, IL-18 expression was consistently upregulated in the Eimeria challenged birds due to β-glucan exposure. IL-4 expression was downregulated in the non-challenged birds fed the 0.1% β-glucan diet. Mucin-1 expression was significantly decreased due to 0.1% β-glucan supplementation. On d 14, mucin-2 expression was decreased due to the Eimeria infection in the 0.1% β-glucan fed birds. Though not significant, there was a tendency for birds fed 0.1% β-glucan to express lower levels of IL-13 than the control birds. Taken together, the data provided from these trials strongly suggest that β-glucans downregulate T helper type 2 cytokines and thus favor a T helper type 1 cell response.