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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #185938
Title: COMPARISON OF ERK 1/2, P38 MAPK, AND PTK KINASE ACTIVITY IN HETEROPHILS FROM WILD-TYPE TURKEYS TO ACTIVITY IN HETEROPHILS FROM A COMMERCIAL TURKEY LINE

Author
item Genovese, Kenneth - Ken
item LOWRY, VIRGINIA - TX A&M UNIVERSITY
item He, Louis
item Nisbet, David
item Kogut, Michael - Mike

Submitted to: Keystone Symposia
Publication Type: Abstract Only
Publication Acceptance Date: 11/10/2006
Publication Date: 2/10/2006
Citation: Genovese, K.J., Lowry, V.K., He, H., Nisbet, D.J., Kogut, M.H. 2006. Comparison of ERK1/2, p38 MAPK, and PTK activity in heterophils from wild-type turkeys to heterophils from a commercial turkey line [abstract]. Innate Immunity Keystone Symposia. p. 60.

Interpretive Summary:

Technical Abstract: Heterophils isolated from wild-type Rio Grande turkeys and a commercial line of turkeys (Line A) on days 4 and 7 post-hatch were stimulated for 1 hr with either nonopsonized Salmonella enteritidis (SE) or opsonized SE (OPSE). After stimulation, cell supernatants were tested for erk 1/2, p38 MAPK, and protein tyrosine kinase activity using commercially available ELISA kits. On both day 4 and day 7, heterophils from the wild turkeys had significantly higher levels of erk 1/2 and p38 MAPK kinase activity following stimulation with phagocytic agonists. Likewise, PTK values in heterophils from Rio Grande turkeys were significantly higher upon stimulation than was measured in the heterophils from the domesticated, commercial turkeys. Combined with our previous studies, the data here suggests that greater heterophil functional activity in Rio Grande turkeys than in commercial lines of turkey’s results from a more efficient activation of the MAPK signaling cascade. Moreover, the data implies that selection of commercial lines of turkeys for larger, heavier bodies, and faster growth is linked to a decreased ability to activate the MAPK pathways resulting in decreased innate immune functions and an increased susceptibility to disease.