Skip to main content
ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Infectious Bacterial Diseases Research » Research » Publications at this Location » Publication #241540

Title: Unraveling the Host Response to Mycobacterium avium subsp. paratuberculosis: One Thread at a Time

item Stabel, Judith

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 6/9/2009
Publication Date: 8/9/2009
Citation: Stabel, J.R. 2009. Unraveling the Host Response to Mycobacterium avium subsp. paratuberculosis: One Thread at a Time [abstract]. International Colloquim on Paratuberculosis. p. 67.

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. Improved tools for the measurement of immunologic responses in ruminant species, particularly the bovine, a key target species for MAP infection, has allowed the dissection of host immunologic responses to infection to some extent. 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. Due to the intracellular nature of MAP, the macrophage is the first defense against infection. However, MAP is able to disarm host defense mechanisms and survive within cells of key target tissues. This disarmament is likely due to the provocation of immune mediators that may be immunosuppressive in nature. Cytokines such as IL-10 and TGF-beta have been shown to mediate immunosuppression due to their inhibitory effects on CD4+ T cell activation and IFN-gamma production. However, the dynamic between macrophages (APCs), T cells, and potentially B cells cannot be so easily explained, as a multifactorial dysregulation of host immunity is likely.