Administration of Salmonella enteritidis-immune lymphokine to day-old turkeys by subcutaneous, oral, and nasal routes: A comparison of effects on Salmonella enteritidis liver invasion, peripheral blood heterophilia and heterophil activation.

ABSTRACT

Previous experiments have shown that the administration by intraperitoncal (i.p.) injection of Salmonella enteritidis-immune Iymphokines (LK) derived from chicken splenic T cells protect both chicks and turkey poults from Salmonella enteritidis (SE) organ invasion. This protection was mediated by the avian heterophil. The present experiments evaluated the ability of SE-immune Iymphokines derived from a virally transformed chicken T cell line (VILK) in protecting day-old turkeys against SE liver invasion, inducing peripheral blood heterophilia, and functionally activating heterophils when delivered by subcutaneous (s.c), oral (p.o.) or intranasal (i.n.) routes when compared to i.p. injection. All routes of administration of VILK showed dramatic reductions in SE liver invasion (P < 0.01) and significant elevations in the number of heterophils in the peripheral blood (P < 0.01). The rise in peripheral blood heterophils was accompanied by a significant increase in the functional activity of the heterophils. Chemotactic movement of heterophils from all VILK groups was two to three times that observed in the control heterophils using chicken serum and recombinant human interleukin-8 (rhuIL-8) as the chemoattractants (P<0.01). The number of heterophils phagocytizing SE and the number of bacteria per heterophil were significantly higher in all VILK administered groups (P < 0.01). Adherence to bovine serum albumin (BSA) revealed significant increases in adherence of heterophils from all VILK administered groups when compared to control heterophils from poults (P<0.01). The results of these experiments clearly show that VILK delivered s.c, p.o. and i.n. is as effective in protecting day-old poults from SE invasion as an i.p. injection and that this protection is also mediated by the activation of an increased number of heterophils in the circulation.