Submitted to: Comparative Immunology Microbiology and Infectious Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/26/2001
Publication Date: 3/1/2002
Citation: N/A Interpretive Summary: During the first week of life after hatching, the immune system of the baby chick is not very good at fighting infections caused by bacteria like Salmonella. However, by giving the baby chicks fluids from white blood cells from adult chickens (ILK) that are immune to Salmonella we can prevent infections in the baby chicks. This protection is caused by a type of white blood cell called the heterophil. The objective of this experiment was to look at what causes the heterophil to move from the blood of the chick to the gut which is where the bacterial infection occurs. We found that after treating the chicks with ILK, the cells of the gut produce a product called interlukin-8 (IL-8) that attracts the heterophils to the gut. Once in the gut, these cells kill the Salmonella. These experiments are important to the pharmaceutical industry because we have found a way to stimulate production of IL-8 which will protect the baby chicks from Salmonella infections.
Technical Abstract: Increased resistance to Salmonella enteritidis (SE) organ infectivity in chickens can be conferred by the prophylactic administration of SE-immune lymphokines (ILK). Resistance is associated with an enhanced heterophilic accumulation within 4 hours of ILK injection. In these studies, we investigated the role of IL-8 in ILK-mediated heterophil recruitment during SE infections in young chickens. Heterophil accumulation was enhanced 2-4 h after the i.p. injection of both ILK and SE (ILK/SE) when compared to the control chicks. An i.p. injection of a rabbit polyclonal anti-human IL-8 antibody significantly (P < 0.01) reduced the accumulation of heterophils in the peritoneum after the injection of ILK/SE. Injections of pre-immune rabbit IgG had no effect on peritoneal heterophil numbers. Within 2 h of injection of ILK/SE, a ten-fold increase in heterophil chemotactic activity was found in the peritoneal lavage fluid from these chicks compared to the saline control chicks. Pre-treatment, with the anti-IL-8 antibody, of the peritoneal lavage fluids collected from the ILK/SE-treated chicks dramatically reduced this heterophil chemotactic activity. Treatment of the lavage fluids from all groups with pre-immune IgG had no effect on heterophil chemotaxis. Additionally, pre- treatment of ILK with the anti-human IL-8 antibody had no effect on heterophil chemotaxis. The results from these experiments suggest that IL-8 is produced locally by the host in response to both the SE infection and the ILK. With these studies, we have established that IL-8 is a major chemotactic factor produced by the host which aids in mediating the ILK/SE-induced recruitment of heterophils to the site of SE invasion.