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.
Animals Arachidonic Acid