Submitted to: Poultry Science
Publication Type: Peer reviewed journal
Publication Acceptance Date: 5/2/2001
Publication Date: N/A
Citation: Interpretive Summary: Ability of poultry to mount an effective immune response depends upon successful interaction of neuroendocrine and immune system. In this report, ARS scientist in collaboration with scientists at the Pennsylvania Stata University and Virginia Commonwealth University, demonstrate ways how different stimuli induce host immune response in chickens. They show that early production of chicken cytokines such as IL-1 is important for successful host immune response to pathogens. Understanding the factors which trigger effective poultry immune response will lead to a better management of poultry health by poultry industry and will reduce economic losses due to diseases.
Technical Abstract: The interaction between the components of the immune and endocrine systems can control the outcome of the immune response. The purpose of the present study was to investigate the role of different cytokines and hormones in the initiation of humoral immunity. Immature Cornell K-strain male chickens were injected i.v. with 8mg/kg BW of lipopolysaccharide (LPS) from Escherichia coli, a T-independent antigen or with 40mg/kg BW bovine serum albumin (BSA), a T-dependent antigen. Control birds were injected with 0.9% saline. Blood and spleens were collected at 0, 1, 3, 6, and 24 h following the injections. The blood was centrifuged and the plasma was collected. Plasma samples were assayed for Interleukin-1 (IL-1) like activity using the thymocyte co-mitogensis assay following the precipitation of inhibitory factors with polyethylene glycol. Tumor necrosis factor-a (TNF-a ) like activity was measured as cytotoxic activity against the L929 mouse fibroblast cell line. The plasma was also assayed for corticosterone and tri-iodothyronine (T3) by radioimmunoassays. Interleukin-2 (IL-2) activity was measured in the conditioned medium from splenic lymphocytes following their stimulation with the T-cell mitogen Concanavalin-A (Con-A) for 24 h.