Longevity of augmented phagocytic activity of heterophils in neonatal chickens following administration of Salmonella enteritidis-immune lymphokines to chickens.

Previously, our laboratory reported an existing relationship between ontogenesis of heterophil activity and susceptibility to Salmonella enteritidis infection in poultry during the first week post-hatch. The prophylactic administration of S. enteritidis-immune lymphokines has been shown to enhance heterophil function in vitro and reduce S. enteritidis organ invasion in 1-day-old chicks. However, how long the heterophils remain activated is currently unknown. The objective of this research was to evaluate the duration of enhanced heterophil phagocytosis of S. enteritidis following the prophylactic administration of a single injection of S. enteritidis-immune lymphokines to neonatal chicks. Administration of S. enteritidis-immune lymphokines on the day of hatch resulted in a significant increase in heterophil phagocytic activity (P < 0.05) through day 5 post-hatch. No significant differences in phagocytic activities of heterophils from control and S. enteritidis-immune lymphokinetreated chicks was demonstrated from day 6 to 14 post-hatch. These data suggest that the administration of S. enteritidis-immune lymphokines on day of hatch potentiates heterophil phagocytic activity during a critical period of susceptibility to Salmonella infection in neonatal chicks. The immune lymphokine-induced enhancement of heterophil activity subsides by day 5 as the chick's natural defenses mature and are able to resist infections without exogenous augmentation.

Enhancement of phagocytosis and bacterial killing by heterophils from neonatal chicks after administration of Salmonella enteritidis-immune lymphokines.

During the first week post-hatch, chickens demonstrate an increased susceptibility to infection by bacteria such as Salmonella. The purpose of the present study was to evaluate the effects of immune lymphokines on phagocytosis and killing activities of heterophils in chicks during the first 1-7 days of life. Lymphokines isolated from chicken splenic T-cells harvested from Salmonella enteriditis (SE)-hyperimmunized hens (SE-ILK), have in past experiments, demonstrated augmentation of heterophil activity in day-of-hatch chicks resulting in protection from SE organ invasion. The present experiments reveal significant increases (p<0.05) in heterophil phagocytosis and killing when comparing chicks treated with SE-ILK to control groups in vitro. In SE-ILK-treated groups, a two-fold or greater increase is noted in heterophil phagocytosis within I h of incubation as compared to controls. Heterophils isolated from 1-day-old and 4-day-old chicks treated with SE-ILK killed significantly greater numbers (p<0.05) of SE than heterophils isolated from control groups. By Day 7 post-hatch, significance is not noted in the killing activity of heterophils from treated groups when compared to control groups. However, heterophils from SE-ILK groups continue to kill greater numbers of SE than control groups. These data support SE-ILK augmentation results in an enhanced heterophil function in chicks during the greatest period of susceptibility to Salmonella invasion.

Resistance to Salmonella enteritidis organ invasion in day-old turkeys and chickens by transformed T-cell line-produced lymphokines.

We previously reported an increased resistance to Salmonella enteritidis (SE) organ invasion in chicks and turkey poults injected prophylactically with SE-immune lymphokines (ILK). In the present study, concanavalin A (Con-A)-activated splenic T cells isolated from SE-hyperimmunized hens were transformed in vitro with reticuloendotheliosis virus strain T (REV-T) (chicken syncitial virus). These transformed T cells were then maintained as a long-term (> 1 yr) cell line for the harvest of immune lymphokines (VILK). The efficacy of VILK to protect turkey poults and chicks against SE organ invasion and the correlation between organ invasion and peripheral blood heterophilia were then evaluated. Three groups of day-old poults and chicks were injected intraperitoneally with either phosphate-buffered saline (PBS; group A), ILK (group B), or VILK (group C). Thirty minutes postinjection, poults and chicks were challenged per os with 5 x 10(5) colony-forming units (CFU) SE and 5 x 10(4) CFU SE, respectively. At 24 hr posttreatment, birds in groups A, B, and C were euthanatized and liver samples were cultured for the presence of SE. Both the VILK- and ILK-treated turkeys and chicks had significant reductions in organ invasion when compared with the PBS-injected controls (P < 0.005). For peripheral blood studies, turkeys and chicks were treated as above, and at 4 hr post-PBS, ILK, or VILK injection; total and differential peripheral blood counts were performed on birds from each group. A significant (P < 0.05) peripheral blood heterophilia at 4 hr postinjection was observed in the ILK- and VILK-treated birds, with no such increase found in the PBS-injected group. Correlation analysis revealed a direct relationship between the peripheral blood heterophilia in turkeys and chicks seen at 4 hr postinjection and the reduction in SE organ invasion seen in the VILK and ILK treatment groups (r = 0.991, r = 0.91, respectively). T cells isolated and transformed from nonimmune chickens did not produce factors that protected chicks from SE organ invasion and did not cause the peripheral blood heterophilia observed with ILK and VILK. These results show that the virally transformed SE-immune T-cell line produces lymphokines that result in the same level of peripheral blood heterophilia as ILK and was equally protective against SE organ invasion as ILK.