Location: Infectious Bacterial Diseases ResearchTitle: Cellular Interactions in Mycobacterium avium subsp. paratuberculosis Infection) Author
Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 7/1/2010
Publication Date: 10/5/2010
Citation: Stabel, J.R. 2010. Cellular Interactions in Mycobacterium avium subsp. paratuberculosis Infection [abstract]. Pathogenesis of Bacterial Diseases of Animals. p. 42. Interpretive Summary:
Technical Abstract: The study of host immune responses to Mycobacterium avium subsp. paratuberculosis (MAP) is complicated by a number of factors, including the protracted nature of the disease and the stealthy nature of the pathogen. Noted as one of the more fastidious mycobacteria, infection with MAP is often characterized by periods of subclinical infection extending for 3 to 5 years. Many animals will clear the infection during this period but it is almost impossible to distinguish by current methods animals that have cleared the infection from those that remain infected but are able to control the progression of disease. Escalation of paratuberculosis to a more clinical state, marked by diarrhea and weight loss, is thought be caused by immune dysfunction. Early measures of host immune responses to infection with mycobacterium, including MAP, have been dominated by a strong bias towards Th1-mediated IFN-gamma production. Since IFN-gamma is a key effector cytokine involved in the activation of T cells and macrophages, maturation of dendritic cells, upregulation of MHC I and II molecules, and production of reactive oxygen and nitrogen species by macrophages, it is purported to be not only an immune response variable but also a correlate of immune protection. However, it is unlikely that the paradigm of host immune responses in the early stages of infection and subsequent resistance to infection is quite so simplistic. Rather, a complex coordination of immune responses is more probable, with these responses shifting as the host transitions through the different stages of infection and disease (subclinical to clinical).