A mucosal immune response induced by oral administration of heat-killed Mycobacterium avium subsp. paratuberculosis
Davide Cossu1, Kazumasa Yokoyama2, Tamami Sakanishi3
1Juntendo University, Department of Neurology, Tokyo 113-8431, Japan; Juntendo University, Advanced Research Institute for Health Science, Tokyo 113-8431, Japan.
Abstract:
Findings in humans and animals have demonstrated a potential role for Mycobacterium avium subsp. paratuberculosis (MAP) antigenic components in encephalitogenic T cell activation. Here we reported that oral administration of MAP activates the mucosal immunity and exacerbates active experimental autoimmune encephalomyelitis (EAE) in C57BL/6J mice, modulating the immune cell traffic from secondary lymphoid organs to central nervous system. The detection of antigenic mycobacterial components by intestinal antigen-presenting cells may modulate the immune system and the subsequent inflammatory status through various signaling mechanisms, including the synthesis of pro-inflammatory cytokines involved in EAE pathogenesis.
Insights
Mycobacterium avium subsp. paratuberculosis (MAP) components activate mucosal immunity and worsen experimental autoimmune encephalomyelitis (EAE) by altering immune cell movement to the central nervous system.
Area of Science:
- Immunology
- Neuroscience
- Microbiology
Background:
- Mycobacterium avium subsp. paratuberculosis (MAP) antigenic components are implicated in T cell activation relevant to encephalomyelitis.
- Experimental autoimmune encephalomyelitis (EAE) is a model for studying central nervous system inflammatory diseases.
Purpose of the Study:
- To investigate the effect of oral MAP administration on mucosal immunity and EAE in mice.
- To elucidate the mechanisms by which MAP influences immune cell trafficking and central nervous system inflammation.
Main Methods:
- Oral administration of MAP to C57BL/6J mice.
- Induction and assessment of experimental autoimmune encephalomyelitis (EAE).
- Analysis of immune cell populations and cytokine profiles.
Main Results:
- Oral MAP administration activated mucosal immunity.
- MAP exacerbated active EAE in C57BL/6J mice.
- MAP modulated immune cell traffic from lymphoid organs to the central nervous system, involving pro-inflammatory cytokine synthesis.
Conclusions:
- Oral MAP components can activate mucosal immunity and worsen EAE.
- MAP influences immune responses and central nervous system inflammation through antigen presentation and cytokine signaling.
