|Sweeney, R - UNIV. OF PA|
|Whitlock, R - UNIV. OF PA|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: March 6, 2008
Publication Date: April 18, 2008
Citation: Sweeney, R.W., Stabel, J.R., Whitlock, R.H. 2008. Immune Response to Orally Administered Killed MAP in Calves [abstract]. Johne's Disease Integrated Program. Technical Abstract: The objective of this study was to determine whether orally administered heat-killed MAP could induce a protective immune response in calves. Newborn male dairy calves were randomly assigned to one of 4 treatment groups: Heat killed MAP only (n=2), live MAP challenge only (n=4), heat killed MAP followed by live MAP challenge (n=4), and untreated controls (n=2). Calves were given 10^8 CFU of heat killed field strain isolate of MAP (or placebo) orally at 7 and 21 days of age, and given a live challenge of 2x10^8 CFU/day MAP orally on two consecutive days at 35 days of age. Calves were euthanized 7 weeks after the live MAP challenge. Supernatants from PBL and mesenteric lymph node cell cultures, collected at the end of the study, were assayed by ELISA for IFN-gamma and IL-10 following stimulation in-vitro with MAP antigens. Intestinal tissues and corresponding mesenteric lymph nodes (MLN) harvested at post-mortem were cultured for MAP on HEYM. Following in-vitro stimulation with MAP antigens, there were no differences between groups in IL-10 concentration from supernatants of PBL or mesenteric lymph node cells. Concentrations of IFN-gamma from supernatants of PBL and MLN cells were approximately 2- to 16-fold higher in the 3 treatment groups compared with controls, but the differences were not significant. In the calves that received the killed MAP only, the induction of in-vitro IFN-gamma production appeared greater in MLN cells (16-fold higher than controls) than PBL (2-fold higher than controls), whereas in calves that received live MAP, responses in PBL were comparable to MLN cells. There were no differences in the number of tissues culture-positive for MAP, nor for the total number of CFU/tissue between the two live challenge groups. In summary, heat killed MAP did appear to induce antigen specific IFN-gamma production in PBL and mesenteric lymph node cells of calves following oral administration. This response appeared greater in mesenteric lymph node cells than PBLs, when only heat-killed MAP was given. Differences between groups were not statistically significant in part due to the small number of calves in this pilot study. However, administration of heat-killed MAP did not appear to result in reduced tissue colonization with MAP after subsequent live MAP challenge.