Submitted to: Developmental and Comparative Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 15, 2003
Publication Date: April 15, 2003
Citation: CRIPPEN,T.L., HE,H. ., SHEFFIELD,C.L., LOWRY,V.K., KOGUT,M.H., DIFFERENTIAL NITRIC OXIDE PRODUCTION BY CHICKEN IMMUNE CELLS, INFLAMMATION, 27: 603-610, 2003. Interpretive Summary: The presence of bacteria in commercial chicken products can occur when chickens are infected with bacteria prior to processing. The immune system of chickens is the main source of defense against bacterial infections in birds, but the way their immune system works is poorly understood. Phagocytes are a type of blood cell in the immune system that combat bacterial invasion in chickens. The purpose of this study was to better define the defensive mechanisms by which phagocytes ward off bacteria. We found that nitric oxide production, an important defensive mechanism against bacteria, was utilized more by some immune cell types than others. Understanding the role of chicken blood cells in the defense against bacterial infection will lead to the development of methods to boost the immune defensive capabilities of chickens and help us to raise healthier chickens. This may decrease human sickness and death related to bacterial contamination of poultry products.
Technical Abstract: Nitric oxide is a rapidly reacting free radical which has cytotoxic effects during inflammatory responses and regulatory effects as a component of signal transduction cascades. We quantified the production of nitrite, a stable metabolite of nitric oxide, in chicken heterophils, monocytes and macrophages after stimulation by IFN?, LPS and killed bacteria. Our results demonstrate a differential production of nitrite over 72 hours by chicken peripheral blood heterophils, monocytes and the chicken macrophage cell line (HD11). HD11 cells produced an average of 10 fold more nitrite in comparison to monocytes and 30 fold more than heterophils upon stimulation. This production could be inhibited by S-methylisothiourea indicating that the inducible nitric oxide synthase enzyme was participating in the pathway leading to nitrite production. The production could not be increased by treatment with superoxide dismutase demonstrating that nitric oxide is not being scavenged by superoxide.