Abstract
The gastrointestinal disease of ruminants is clinically known as Johne's disease (JD) and is caused by Mycobacterium avium subspecies paratuberculosis (MAP). An accumulative effect by insensitive diagnostic tools, a long subclinical stage of infection, and lack of effective vaccines have made the control of JD difficult. Currently lacking in the model systems of JD are undefined correlates of protection and the sources of inflammation due to JD. As an alternative to commonly studied immune responses, such as the Th1/Th2 paradigm, a non-classical Th17 immune response to MAP has been suggested. Indeed MAP antigens induce mRNAs encoding the Th17-associated cytokines IL-17A, IL-17F, IL-22, IL-23, IL-27, and IFNγ in CD3+ T cell cultures as determined by RT-qPCR. Although not as robust as when cultured with monocyte-derived macrophages (MDMs), MAP is able to stimulate the upregulation of these cytokines from sorted CD3+ T cells in the absence of antigen-presenting cells (APCs). CD4+ and CD8+ T cells are the main contributors of IL-17A and IL-22 in the absence of APCs. However, MAP-stimulated MDMs are the main contributor of IL-23. In vivo, JD+ cows have more circulating IL-23 than JD– cows, suggesting that this proinflammatory cytokine may be important in the etiology of JD. Our data in this study continue to suggest that Th17-like cells and associated cytokines may indeed play an important role in the immune responses to MAP infection and the development or control of JD.
Highlights
Mycobacterium avium subspecies paratuberculosis (MAP) is the causative agent for the clinical onset of Johne’s disease (JD) in ruminants
CD3+ T Cells Cocultured With Monocyte-Derived Macrophages
To further understand the relationship between monocyte-derived macrophages (MDMs) plus CD3+ T cells and IL-23, IL-17A, and IL-22 in regard to a MAPstimulated Th17 response, 5-day old MDMs were cocultured with autologous MAC sorted CD3+ T cells and stimulated with MAP antigen for 18 h
Summary
Mycobacterium avium subspecies paratuberculosis (MAP) is the causative agent for the clinical onset of Johne’s disease (JD) in ruminants. A MAP infection of the ileum leads to chronic diarrhea and reduces the ability of an animal to absorb nutrients due to inflammation and disruption of the intestinal lining. Clinical JD leads to early culling, reduced milk production, and/or premature death. The cumulative effects of JD are a rising concern to both the animal welfare and the dairy industry. Dairy operations infected with MAP may have risen by ∼23% from 2007 to 2013 (68 to 91%) according to the National Animal Health Monitoring System and more recent studies [NAHMS; [1, 2]]. The resulting growth in JD–impacted dairy operations may have concurrently
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