|Kogut, Michael - Mike|
Submitted to: Avian Immunology Group Meeting
Publication Type: Review Article
Publication Acceptance Date: 3/16/1996
Publication Date: N/A
Citation: N/A Interpretive Summary:
Technical Abstract: This is a review of research using avian cytokines as the stimulators of a vigorous inflammatory response in young chicks which results in the resistance of these birds to systemic salmonella infections. Our laboratory has provided convincing evidence linking the resistance of poultry to systemic Salmonella infection with the prophylactic administration of cytokines from S. enteritidis-immune chicken T lymphocytes and the accumulation of inflammatory heterophils at the site of bacterial invasion in the intestine. The presence of a cytokine network during the expression of this anti-Salmonella resistance is pivotal to the initiation and propagation of the protective inflammatory response. The working paradigm that we have developed to describe the initiation of a cytokine cascade consists of at least five steps: 1) localized TNF produced following the administration of SE-ILK and challenge with salmonellae; 2) an IL-8-like chemotactic protein is produced which is responsible for the chemotaxis of heterophils to the site of bacterial invasion; 3) a significant enhancement of biological effector functions of circulating heterophils is induced; 4) a four-fold increase in the PMN- derived adhesion molecule, CD11b/CD18, expression was found on heterophils from the SE-ILK-treated birds which are essential for extravasation and sequestration of the PMNs at the inflamed site; and 5) the massive influx of inflammatory heterophils into the inflamed site. The impressive degree of inflammatory heterophil influx to the site of inflammation results from the diapedesis and migration of these activated cells out of the blood. Additionally, these peritoneal heterophils possess IL-8 receptors which are required for their continued migration to the inflamed site.