Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: October 5, 2005
Publication Date: December 5, 2005
Citation: Stabel, J.R. 2005. Mycobacterium avium subsp. paratuberculosis: The Host Response to a Mighty Foe [abstract]. Research Workers in Animal Diseases Conference Proceedings. p. 112. Technical Abstract: Paratuberculosis (Johne's disease) is a chronic, progressive enteric disease of ruminants caused by infection with Mycobacterium avium subsp. paratuberculosis (MAP). Host immunity to mycobacterial infections are characterized by reciprocal T cell responsiveness associated with the extent of disease. This is observed during infection with MAP as well, with early subclinical infections associated with strong Th1-mediated immunity that serves to control bacterial replication within the host, progressing to full-blown clinical disease associated with reduced Th1 immunity and strong Th2-modulated immune function. Although a mechanism(s) has not been identified for this Th1-Th2 transition, the decrease in IFN-gamma noted during the clinical stage signals a disruption in the effector phase of the host immunity. Recently, we reported that the immunomodulatory cytokines, TGF-beta and IL-10, were upregulated in the tissues of cows with clinical Johne's disease. We also demonstrated increased secretion of IL-10 and TGF-beta by peripheral blood mononuclear cells after stimulation with live MAP. We further demonstrated that adding exogenous IL-10 and TGF-beta to peripheral blood mononuclear cell cultures inhibited the bactericidal activity of these cells as evidenced by increased recovery of viable MAP from the cultures. The presence of these anti-inflammatory cytokines that modulate the effects of pro-inflammatory cytokines such as IFN-gamma might be one mechanism that enhances the survival of mycobacteria within the host.