|Kogut, Michael - Mike|
Submitted to: Journal of Inflammation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/19/1996
Publication Date: N/A
Citation: N/A Interpretive Summary: Poultry products have been shown to be contaminated with Salmonella and food safety has become a major concern to the industry. Salmonella enteritidis (SE) is one of many different bacteria that can infect poultry. We and others have been conducting tests to understand how this bacteria enters the baby chicks body from the intestine and to develop ways sto block the invasion of this bacteria. The chicken's immune system seems to play a major role in preventing this invasion process from the intestine. When we inject baby chicks with proteins from the immune system of other chickens that have already had SE, they protect the new chicks from invasion of this bacteria. The objective of the tests here was to identify which protein causes the protection in baby chicks against SE. We found that a specific protein causes an increase in a specialized white blood cell, the heterophil, which eats and destroys large numbers of SE before they can make the chicken sick. The results from these tests are significant to both the poultry and poultry pharmaceutical industries because we have shown what specific protein of the immune system can be added to new chicks which can prevent SE invasion in these new chicks.
Technical Abstract: Hematopoietic colony stimulating factors (CSF) regulate the growth and development of phagocytic cell progenitors and also augment functional activation of phagocytes. Granulocyte-CSF (G-CSF) is the CSF that acts specifically upon granulocyte progenitor cells and mature granulocytes. We have shown that lymphokines (ILK) from T cells of birds immunized against Salmonella enteritidis (SE) induce a granulocytic (PMN) inflammatory response in chicks challenged with SE . This inflammatory response was characterized by: (a) a dramatic emigration of granulocytic cells from the bone marrow into the peripheral blood, (b) an enhancement of the biological functions of the circulating PMNs, and (c) a directed influx of these activated PMNs to the site of bacterial invasion. In the current study, we determined the presence of G-CSF in ILK by Western blot analysis using a goat polyclonal anti-human G-CSF antibody (Ab). Using this Ab, we then evaluated the role of G-CSF in the ILK-induced protective inflammatory response in chickens against SE. Pretreatment of ILK with the Ab totally abolished the colony-stimulating activity of the ILK. Furthermore, Ab treatment of ILK resulted in: (a) an elimination of the ILK-induced peripheral blood heterophilia with a dramatic inhibition of ILK-mediated protection against SE organ invasion and (b) an elimination of accumulation of inflammatory PMNs in the peritoneum with subsequent decrease in the survival rate of chicks challenged ip with SE. Taken together these studies demonstrate for the first time the contribution of G-CSF to avian PMN activation and the immunoprophylaxis of SE infection by ILK in neonatal chickens.