Submitted to: Developmental and Comparative Immunology
Publication Type: Abstract Only
Publication Acceptance Date: 6/30/2003
Publication Date: N/A
Citation: N/A Interpretive Summary:
Technical Abstract: We have previously reported the inhibition of Fc receptor-mediated degranulation in avian heterophils by the syk tyrosine kinase inhibitor piceatannol. The present studies investigated whether attachment of complement opsonized bacteria to complement receptors also involve the syk tyrosine kinase pathway in the oxidative burst of heterophils derived from day-old chickens. Complement opsonized Salmonella enteritidis was added to heterophils previously exposed to piceatannol at increasing concentrations (12.5, 25, and 50 uM piceatannol). After one hour incubation at 39 deg C, the oxidative burst of heterophils was measured by luminal-dependent chemiluminescence. Data for 4 repetitions were pooled and the oxidative burst of piceatannol-treated heterophils was expressed as a percentage of the oxidative burst of untreated control heterophils exposed to complement opsonized SE. As seen with Fc receptor-mediated heterophil degranulation, piceatannol treatment resulted in a dose-dependent reduction in the oxidative burst of treated heterophils. At a concentration of 50 uM piceatannol, the oxidative burst was reduced to 16.5 % of the oxidative burst observed in control heterophils. These experiments will aid in further experiments designed to describe the pathway of signal transduction incurred by the attachment of complement opsonized bacteria to the surface of the avian heterophil and the resulting oxidative burst and killing of the phagocytized bacteria.