ARS | Publication request: DIFFERENTIAL HETEROPHIL INTRACELLULAR SIGNALING AND FUNCTIONS IN WILD-TYPE AND COMMERCIAL TURKEYS

Submitted to: Avian Immunology Research Group Abstract
Publication Type: Abstract Only
Publication Acceptance Date: June 20, 2006
Publication Date: October 21, 2006
Citation: Genovese, K.J., He, H., Swaggerty, C.L., Kogut, M.H. 2006. Differential heterophil intracellular signaling and functions in wild-type and commercial turkeys [abstract]. In: Proceedings of 09th Avian Immunology Research Group Meeting, October 21-24, 2006, Paris, France. p. 51.

Technical Abstract: A comparison of cell signaling and functions in heterophils from a commercial line (A) to wild-type Rio Grande turkeys days 4 and 7 post-hatch was conducted. Mitogen-activated protein kinases (MAPK) p38 and ERK 1/2 and total protein tyrosine kinase (PTK) activities were measured. After stimulation with Salmonella (SE) or opsonized SE (OPSE), heterophils were lysed, and resulting cell lysates tested for MAPK and PTK activity using a commercial ELISA. Day 4 and 7 post-hatch, Rio Grande heterophils had significantly higher levels of ERK 1/2 and p38 MAPK kinase activity upon stimulation with SE and OPSE. PTK values on day 4 and 7 post-hatch in Rio Grande heterophils was significantly higher upon stimulation with SE than with OPSE and was significantly higher than the PTK levels in Line A upon SE and OPSE stimulation. Heterophil phagocytosis of SE and two mechanisms of microbial killing, oxidative burst and degranulation, were assayed. Heterophils from wild-type turkeys had a significantly greater production of an oxidative burst and degranulation on days 4 and 7 post-hatch than did heterophils from Line A. No differences in the phagocytosis of SE were observed between lines. In combination, these results show that heterophils from wild-type turkeys function more efficiently than do heterophils from commercial Line A turkeys and that the efficiency of cellular function observed in heterophils from Line A turkeys may be associated with defects or insufficiencies in the intracellular signaling mechanisms related to the innate immune response.