Submitted to: Journal of Interferon Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/20/1995
Publication Date: N/A
Citation: N/A Interpretive Summary: In the last 10-12 years, many studies have shown that a large percentage of poultry products are contaminated with salmonellae. As a result, food safety has become a major concern to the poultry industry. Salmonella enteritidis (SE) has been found to be the most prevalent bacterial contaminant of poultry products. Our laboratory is developing ways to stimulate the immune system of the baby chick in order to make it more resistant to SE and other salmonellae. Recently, studies from our laboratory have shown that products called lymphokines, produced by a white blood cell (T lymphocyte) from chickens that are immune to SE, can protect baby chicks from SE infection. The objective of this experiment was to identify a possible component contained in these lymphokines, specifically colony-stimulating factor. The results showed that the lymphokines contained large amounts of colony-stimulating factor (CSF) and that this CSF causes the chick to produce large numbers of protective whit blood cells called heterophils. These results are important to both the animal health and poultry industries because we now have identified a major component of the lymphokines which can now be purified and used to protect chicks from SE infection early in life.
Technical Abstract: Granulocyte- and granulocyte- macrophage-colony-stimulating factors (CSF) are cytokines that induce myelopoiesis, prime polymorphonuclear leukocyte (PMN) function, and cause a PMN-predominated leukocytosis. Previously administration of conditioned medium of concanavalian A-stimulated avian T-cells from Salmonella enteritidis- (SE) immune chickens (SE-immune lymphokine; ILK) increased circulating PMNs in SE-challenged chicks. Current objectives were to (a) determine whether colony- stimulating activity (CSA) was present in ILK, (b) determine types of colonies from the bone marrow that were supported in vitro by the potential CSF in ILK, and (c) determine whether CSA was present in serum from ILK-treated, SE- challenged chicks, and (d) use physiochemical treatments to identify potential CSF in ILK. ILK alone and serum from ILK-treated, SE-challenged chicks significantly increased the number of colony-forming units from bone marrow in vitro. At 10 d of incubation, ILK solely supported the in vitro growth of granulocytic bone marrow colonies. CSA from serum derived from ILK-treated, SE-challenged chicks peaked at 2 h post-challenge. When ILK was treated with either heat (100 C), trypsin, or acid and then injected into chicks, all groups of chicks responded with significant increases in circulating PMNs. When assayed for in vitro CSA, only trypsinization abrogated the CSA in ILK.