Location: Infectious Bacterial Diseases ResearchTitle: The other way around: probiotic Lactobacillus acidophilus NP51 restrict progression of Mycobacterium avium subspecies paratuberculosis (MAP) infection in Balb/c mice via activiation of CD8 alpha+ immune cell-mediated immunity Author
Submitted to: Meeting Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 2/4/2012
Publication Date: 2/19/2012
Citation: Osman, M.A., Stabel, J.R., Hostetter, J.M., Nettleton, D., Ware, D., Beitz, C.D. 2012. The other way around: probiotic Lactobacillus acidophilus NP51 restrict progression of Mycobacterium avium subspecies paratuberculosis (MAP) infection in Balb/c mice via activiation of CD8 alpha+ immune cell-mediated immunity. In: Proceedings of the 11th International Colloquium on Paratuberculosis, February 5-10, 2012, Sydney, Australia. p. 129-131. Interpretive Summary: Johne's disease is a chronic, debilitating intestinal disorder in cattle characterized by diarrhea, reduced feed intake, weight loss and death. Cattle usually become infected as young calves by ingesting feces containing the causative bacteria. However, symptoms of disease do not usually present themselves until the animals reach 3 to 5 years of age or even older. During this time the animal is infected and may be shedding the organism in its feces without showing any clinical signs of disease. In addition to reduced milk production by these animals, they also present a potential infective threat to the rest of the herd. Johne’s disease is difficult to diagnose and therefore to control. Development of therapeutic measures is an important management tool that can be used to reduce the spread of this disease. This study demonstrated that feeding a probiotic (nonpathogenic bacterium) to mice stimulates the immune response and, therefore, may help control Johne’s disease. Further work on the utility of probiotics in dairy calves will determine if it is a useful management tool for dairy producers in allaying the spread of infectious disease to their calves and improving their health.
Technical Abstract: The objective of this study was to examine the immune-modulating effects of feeding a 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) in ruminant animals. 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 were either fed the viable or heat-killed NP51 (VNP51 or HNP51, respectively) and challenged with either the viable or the heat-killed MAP (VMAP or HMAP, respectively). Mice were fed 1 × 10**6 CFU of either VNP51 or HNP51•mouse-1•day-1 mixed with standard mouse chow throughout the study. On day 45 of the study, mice were challenged with 1 × 10**8 CFU of VMAP or HMAP injected intraperitonealy. Ten mice from each group were euthanized on days 45, 90, 135, and 180. Spleens were excised and used for an in vitro splenocyte cell cultures that were either stimulated with sonicated MAP antigen or concanavalin A and examined for frequency of T lymphocyte subpopulations. Also, spleens and livers were cultured on HEYM to evaluate effects of VNP51 and HNP51 on tissue MAP burden. The fecal pellets were collected and examined for MAP shedding. VNP51 and HNP51 differentially stimulated the adaptive immunity and decreased MAP tissue burden and shedding of MAP in fecal pellets. With VMAP as the inoculum, both VNP51 and HNP51 stimulated CD8a+ immune cell-mediated immunity and decreased the humoral immunity. When HMAP was used as the inoculum, VNP51 stimulated both the CD8a+ T cell-mediated and humoral immunity. In contrast, HNP51 feeding induced CD8a+ T cell-mediated immunity only as verified by the differential cytokines and immunoglobulin secretion pattern. These data provide persuasive evidence that NP51 has the potency to prevent JD infection in murine model of JD.