Effect of yeast cell product supplementation on broiler cecal microflora species and immune responses during an experimental coccidial infection.

This experiment was conducted to study the effects of whole yeast (Pichia guilliermondii; CitriStim, ADM, Quincy, IL) cell product supplementation on cecal microflora population and intestinal immune parameters in broilers. In the first experiment, birds were fed 0, 0.1, or 0.2% yeast cell wall product for 42 d. Feeding yeast cell wall products decreased (P = 0.03) the proportion of Escherichia coli in the ceca by 31% compared with the control group. The group fed 0.2% yeast cell wall product had a 20% decrease (P = 0.23) in Salmonella population compared with the control group. In the second experiment, birds were fed yeast cell wall product for 21 d and challenged or not challenged with coccidial oocysts, thus resulting in a 2 (0 and 0.2% whole yeast product) × 2 (coccidial challenge and no coccidial challenge) factorial model. Supplementing whole yeast cell wall product prevented a coccidial infection-induced decrease in the Lactobacillus population (P = 0.09) at 12 d postchallenge. Supplementing yeast cell wall product prevented a coccidial infection-induced increase in the Salmonella population (P = 0.08) and E. coli (P = 0.12) at 12 d postchallenge. At 5 d (P < 0.01) and 12 d (P < 0.01) postcoccidial infection, yeast cell wall product supplementation or coccidial infection increased the regulatory T cell (Treg) percentage in the cecal tonsils, whereas yeast cell wall product supplementation in the coccidial-infected group decreased the increase in Treg percentage. At 5 d postcoccidial infection, coccidial infection increased (P = 0.01) the relative amounts of cecal interferon (IFN)γ mRNA. In addition, the yeast cell wall product supplementation in the coccidial-infected groups further increased (P = 0.15) the IFNγ mRNA. It could be concluded that yeast cell wall product supplementation decreased coccidial-infection-induced increase in E. coli and Salmonella colonization and improved IFNγ mRNA amounts after coccidial infection.