Submitted to: Comparative Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 10, 2003
Publication Date: May 2, 2003
Citation: HE,H. ., FARNELL,M.B., KOGUT,M.H., INFLAMMATORY AGONIST STIMULATION AND SIGNAL PATHWAY OF OXIDATIVE BURST IN NEONATAL CHICKEN HETEROPHILS, COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY, Part A 135 (2003) 177-184. Interpretive Summary: One of the white blood cells of the chicken is called the heterophil, and it is important for proper chicken health because it makes compounds that kill disease-causing bacteria. Baby chicks easily get infected by disease-causing bacteria such as Salmonella. We performed experiments to see how the heterophils of the baby chicks make bacteria-killing compounds and what chemicals will influence the process. We found that baby chick heterophils can make bacteria-killing compounds when they are exposed to materials made by disease-causing bacteria. We also found that heterophils produced different amounts of bacteria-killing compounds depending on the strain of bacteria present. Our findings are important to the pharmaceutical industry in the United States because it shows that we can possibly use chemicals to stimulate baby chick heterophils to fight different bacterial infections.
Technical Abstract: A fluorescence microplate assay was adapted to examine the oxidative response by heterophils from neonatal chicks following in vitro stimulation with various inflammatory agonists. Both nonopsonized formalin-killed Salmonella enteritidis and Staphylococcus aureus stimulated significant heterophil oxidative response. Phorbol myristate acetate (PMA) was the most potent stimulant for the chicken heterophil oxidative response, whereas, the bacterial cell surface components lipopolysaccharide (LPS) and lipoteichoic acid (LTA) were less effective. Our results show that protein kinase C (PKC) is an essential component regulating heterophil oxidative response to stimulation by PMA, LPS, LTA and S. enteritidis. However, inhibition of PKC did not affect the oxidative response to stimulation by S. aureus, suggesting differential signaling pathways responsible for the activation of NADPH oxidase by gram-negative S. enteritidis and gram-positive S. aureus. Inhibition of mitogen activated protein (MAP) kinase p38 and extracellular response kinase (ERK) by SB 203580 and PD 098059, respectively, did not inhibit activated oxidative burst.