Characterization of the Pattern of Inflammatory Cell Influx in Chicks Following the Intraperitoneal Administration of Live Salmonella enteritidis and Salmonella enteritidis-Immune Lymphokines

Abstract

We characterized the inflammatory cell influx in day-old chicks induced by the i.p. administration of live Salmonella enteritidis (SE) and lymphokines from concanavalin A-stimulated SE-immune T lymphocytes (ILK). An i.p. injection of ILK along with 5 x 10(3) cfu SE increased the survival rate of chicks 48 h later from 70% (ILK-treated controls) compared with 25% (saline-treated). The injection of both the ILK and live SE (but not formalin-killed SE) resulted in an increased influx of inflammatory heterophils into the peritoneum that peaked at 4 h after the injections with no increase in peritoneal macrophages. The heterophil accumulation was not influenced by polymyxin B, but was sensitive to heat treatment (100 C for 1 h) of the ILK, suggesting that lipopolysaccharide (LPS) did not contribute to the induced accumulation of heterophils. Treatment of the chicks with nordihydroguaiaretic acid or indomethacin did not abrogate the induced heterophil accumulation, suggesting that arachidonic acid metabolites were not involved in the SE/ILK-induced accumulation of peritoneal heterophils. The results from the current studies indicate that 1) ILK-mediated resistance to SE-induced mortality is mediated by a rapid influx of inflammatory heterophils to the site of infection; 2) live SE, during invasion, are vital for the site-directed migration of the heterophils; and 3) the mechanisms of induced heterophil accumulation are unknown but involve neither LPS nor arachidonic acid metabolites.

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.…”

Rapid Expression of Chemokines and Proinflammatory Cytokines in Newly Hatched Chickens Infected withSalmonella entericaSerovar Typhimurium

“…Although not as pronounced as in mammals, infection with Salmonella serovar Typhimurium leads to some diarrhea and intestinal lesions in young chickens (2) and to an influx of heterophils into the gut accompanied by inflammation and damage to villi, but this is not seen with the avian-specific serovar Salmonella enterica serovar Pullorum (4). Heterophils are the avian equivalent of mammalian neutrophils and play a key role in protecting chickens from the development of systemic disease following infection with Salmonella serovar Enteritidis by largely restricting the bacteria to the gut (11,12). However, there are no descriptions, as yet, of the role of cytokines or chemokines during in vivo Salmonella infections of the chicken, though Salmonella infection in an avian in vitro epithelial model has indicated that invasion with both Salmonella serovar Typhimurium and Salmonella serovar Enteritidis induce production of the proinflammatory cytokine IL-6, whereas invasion with the avian-specific serovar Salmonella enterica serovar Gallinarum did not induce IL-6 (9).…”

Cytokines and prevention of infectious diseases in poultry: A review

“…injection of conditioned medium prepared from Con A-stimulated T lymphocytes isolated from the spleen of chickens immunized against Salmonella enteritidis-protected newly hatched chicks from oral or an i.p. challenge with S. enteritidis (McGruder et al, 1993;Kogut et al, 1994a). This protection was also induced in 1-day-old turkey poults (Ziprin et al, 1996).…”

“…Moreover, the protection conferred by the cytokines lasts only 5 to 10 days (McGruder et al, 1995a;Kogut et al, 1996;Genovese et al, 2000). Mechanistically, protection was associated with an enhanced inflammatory response characterized by: (a) a dramatic granulopoiesis with a resultant peripheral blood heterophilia (Kogut et al, 1994b), (b) a potentiatio n of the biological functions of the circulating heterophils including adherence, chemotaxis, phagocytosis, and bacterial killing (Kogut et al, 1995;Moyes et al, 1998), (c) a directed influx of these activated heterophils to the site of bacterial invasion Kogut et al, 1994a), and (d) a direct correlation between the number of peripheral blood heterophils or peritoneal heterophils and protection against SE organ invasion and SEinduced mortality, respectively (Kogut et al, 1994b(Kogut et al, , 1995. The cytokine-mediated functional activation of the heterophils lasts about 5 days, which coincides with the maturation of natural host resistance to salmonellosis (Ziprin et al, 1989).…”