Effects of dietary addition of Actigen® on the performance and immune cell  concentration of broiler chicks challenged with lipopolysaccharide
L. Macalintal, T. Ao, A. Pescatore, A. Cantor, M. Ford, K. Dawson

Mannan-oligosaccharides derived from Saccharomyses cerevisiae cell wall have been found to promote growth and enhance immune responses in food animals. Actigen®, a yeast cell wall derived product, was added at 400g/T to evaluate its effect on growth performance and immune response in broiler chicks challenged with lipopolysaccharide (LPS). Lipopolysaccharide is a component of the outer cell wall membrane of gram-negative bacteria that has been widely used to immunologically stress chickens. Two hundred and eighty chicks, 1 d of age, were utilized with 10 replicate cages of 7 chicks per cage. A 2x2 factorial treatment arrangement was used with diets and LPS challenge as factors. At D7, 2 groups of chicks fed with or without Actigen® were injected intravenously via the jugular vein with 1 mg/ml LPS. At 1 and 14d post LPS injection, serum samples were collected for nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and interleukin 1β (IL1β) quantification using ELISA. Both BW and FI were reduced (P<0.001) due to LPS challenge at d21. At 1d post challenge, there was a significant Actigen® x LPS interaction (P<0.05) for the serum NFκB concentration. Chicks challenged with LPS and not fed Actigen® had a significantly depressed level of serum NFκB. The challenged chicks that were fed the diet with Actigen® did not have this depression in serum NFκB. Actigen® fed birds had higher (P = 0.07) serum IL1β concentration than non-Actigen® fed birds. By14d post LPS challenge, the immune cell production did not differ among treatment groups (P>0.05). Feeding dietary Actigen® altered the pattern of immune cell responses of broilers challenged with LPS. These results indicate that dietary Actigen® can enhance the cell-mediated immune response by modulating the production of inflammatory cytokines during the early phases of inflammation.