|He, Louis - Haiqi|
|Genovese, Kenneth - Ken|
|Swaggerty, Christina - Christi|
|Kogut, Michael - Mike|
Submitted to: Molecular Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/16/2009
Publication Date: 6/1/2009
Citation: He, H., MacKinnon, K.M., Genovese, K.J., Nerren, J.R., Swaggerty, C.L., Nisbet, D.J., Kogut, M.H. Chicken scavenger receptors and their ligand-induced cellular immune responses. Molecular Immunology. 46:2218-2225.
Interpretive Summary: Scavenger receptors are protein molecules that are produced by animals to detect bacteria and fight infections. Those protein molecules are very important because they control the body’s immune responses to bacterial infection. Macrophages, monocytes, and heterophils are important immune cells found in chickens. These chicken immune cells can produce bacterial-killing chemicals to help chickens fight bacterial infections and stay healthy. We found that scavenger receptors help the chicken macrophages produce bacteria-killing chemicals when they are exposed to bacteria and chemicals made by bacteria. Our findings are important to veterinary medicine and to the poultry industry in the United States because it shows that we can possibly use chemicals to stimulate the scavenger receptors of the chicken macrophages to fight bacterial infections more efficiently.
Technical Abstract: The (SRs) comprise structurally and functionally divergent groups of cell surface and secreted proteins that play an important role in innate immune defenses. Searching translated chicken genomic databases revealed many proteins homologous to mammalian SRs. SR mediated immune functions (oxidative burst, degranulation, phagocytosis, nitric oxide (NO) production, and cytokine expression) were evaluated in chicken heterophils, peripheral blood mononuclear cells (PBMC), and a chicken macrophage cell line (HD11) stimulated with various SR class A and B ligands. Results showed that the SR-A ligands, fucoidan, poly(I) and poly(G), but not SR-B ligands, phosphatidylserine, and LDL, stimulated dose-dependent NO production in HD11 cells. However, SR-A ligands failed to induce NO in chicken monocytes. Quantitative RT-PCR indicated that SR ligands differentially regulated the gene expression of cytokines and chemokine in HD11 cells with a strong up-regulation of the cytokines IL-1Beta and IL-6 and the chemokine MIP-1Beta, but had no effect on IL-4, IL-12, IFN-', and IFN-Beta. SR-B ligands did not alter expression of these genes. SR-A ligands had no stimulatory effect on functional response in heterophils. However, LDL, a SR-B ligand, stimulated oxidative burst in both heterophils and PBMC. Additionally, results indicate that SRs are involved in bacterial binding in macrophages.