|OSMAN, A - Iowa State University|
|HOSTETTER, J - Iowa State University|
|NETTLETON, D - Iowa State University|
|WARE, D - Nutrition Physiology Company, Llc (NPC)|
|BEITZ, D - Iowa State University|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2011
Publication Date: 2/19/2012
Citation: Osman, A.M., Stabel, J.R., Hostetter, J.M., Nettleton, D., Ware, D., Beitz, D.C. 2012. The other way around: Probiotic lactobacillus acidophilus NP51 restricts progression of Mycobacterium avium subspecies paratuberculosis (MAP) infection in Balb/c mice through activation of CD8+ T cell-mediated immunity [abstract]. International Colloquium on Paratuberculosis. p. 129.
Technical Abstract: The objective of this study was to examine immune effects of feeding novel probiotic Lactobacillus acidophilus strain NP51 to specific pathogen-free Balb/c mice challenged with Mycobacterium avium subspecies paratuberculosis (MAP), the causative agent of Johne’s disease (JD). We hypothesized that feeding the NP51 would activate the adaptive immunity and impede the development of MAP infection in murine model of JD. Thus, Balb/c mice were randomized to treatment groups in a factorial design including mice that either fed the heat-killed or viable NP51 (HNP51 or VNP51, respectively) and challenged with either a heat-killed or a viable MAP (HMAP or VMAP, respectively). Mice were fed 1 × 10**6 CFU of either HNP51 or VNP51· mice-1 · day-1 mixed with standard mouse chow until the end of the study. Subsequently, mice were challenged with 1 × 10**8 CFU of HMAP or VMAP injected intraperitonealy on day 45 of the study. Ten mice from each group were euthanized on days 45, 90, 135, and 180. Spleens were excised and used for in vitro splenocytes cell cultures that were either stimulated with sonicated MAP antigen or concanavalin A and examined for the cytokine secretion pattern and frequency of T lymphocyte subpopulations. Blood was withdrawn by cardiac puncture and used for examination of immunoglobulins production. VNP51 and HNP51 differentially stimulated the adaptive immunity and decreased tissue MAP burden. With VMAP as the inoculum, both VNP51 and HNP51 stimulated CD8+ T cell-mediated immunity and decreased the humoral immunity. When HMAP was used as the inoculum, VNP51 stimulated both the CD8+ T cell-mediated and the humoral immunity. In contrast, HNP51 feeding induced CD8+ T cell-mediated immunity only as verified by the differential cytokines and immunoglobulins secretion pattern. The data provide conclusive evidence that NP51® has the potency to prevent MAP infection in murine model of JD through activation of the CD8+ T cell-mediated immunity.