In vivo activation of heterophil function in chickens following injection with Salmonella enteritidis-immune lymphokines

Abstract

We have previously shown that increased resistance to Salmonella enteritidis organ infectivity in day-old chicks was conferred by the immunoprophylactic administration of S. enteritidis-immune lymphokines (ILK). This resistance was associated with a significant increase in the number of circulating heterophils 4 h after ILK injection. The objective of the present study was to evaluate heterophil function following the administration of ILK in day-old chicks. Significant increases (P < 0.001) in adherence, chemotaxis, and phagocytosis of S. enteritidis were found with heterophils isolated from ILK-injected chickens compared to the heterophils isolated from birds injected with either pyrogen-free saline or lymphokines from non-immune T cells. After phagocytosis, the heterophils from the ILK-injected chickens were also able to kill significantly greater numbers of S. enteritidis more rapidly than did the heterophils from the saline-injected control birds (within 30 min, control cells killed 21.89% of the bacteria whereas ILK-treated cells killed 88.22%). We also found that the heterophils from the ILK-injected birds were more efficient killers of S. typhimurium, S. gallinarum, and E. coli. These results strongly suggest that the protection against S. enteritidis organ invasion induced by the prophylactic treatment of day-old chicks with ILK involves activated heterophils which migrate rapidly to the inflammatory stimulus where they phagocytize and kill the bacteria.

Differential cytokine expression in avian cells in response to invasion by Salmonella typhimurium, Salmonella enteritidis and Salmonella gallinarum The GenBank accession numbers for the sequences reported in this paper are AI982185 for chicken IL-6 cDNA and AJ250838 for the partial chicken IL-6 genomic sequence, respectively.

“…S. enteritidisimmune lymphokines have been partially characterized and shown to influence an inflammatory response and to activate heterophils (Kogut et al, 1994a(Kogut et al, , b, 1995. However, until the recent progress in cloning avian cytokine genes, it had not been possible to fully characterize these lymphokines due to the lack of avian cytokine reagents.…”

Resistance to Salmonellosis in the Chicken Is Linked toNRAMP1and TNC

“…Chickens are highly susceptible to infection with Salmonella during the first days posthatching, after which they build up their resistance to infection (Gast and Beard 1989). During this early period of life, protection against Salmonella infection involves activated heterophils, the avian equivalents to mammalian neutrophils, which migrate rapidly to the inflammatory site where they phagocyte and destroy opsonized bacteria through an oxygenindependent mechanism (Kogut et al 1995). Resistance of older chickens (4-week-old) to Salmonella infection involves both cellular and humoral immune functions as measured by B and T cell proliferation, antibody responses, and cytotoxic activity of NK cells (Lessard et al 1995).…”

Salmonella infections: immune and non-immune protection with vaccines

“…Another result underlining the importance of chicken heterophils in protection against Salmonella organ invasion was the finding that intraperitoneal administration of S. Enteritidis-immune lymphokines (SE-ILK) to 18-week old chickens protected the animals from organ invasion by S. Enteritidis (Hargis et al, 1999;Tellez et al, 1993). SE-ILK are soluble products produced by Tlymphocytes, derived from S. Enteritidis-immune hens, cultured in the presence of concanavalin A. Intraperitoneal administration of SE-ILK in chickens resulted in a dramatic increase in the number of heterophilic granulocytes into the peritoneum without changing the numbers of other leukocytes and administration in ovo protected young chicks against organ invasion by Salmonella (Kogut et al, 1995a(Kogut et al, , 1995b. These studies indicate not only the importance of this aspect of the innate response to Salmonella infection but also suggest that the course of infections might be modulated by manipulation of these responses.…”