Abstract
Mycobacterium avium subsp. paratuberculosis (MAP) infection is highly spread in the ruminant herds of Sardinia, in the Western Mediterranean. The objective of this study was to investigate prevalence of MAP infection in association with Multiple Sclerosis (MS) using clinical specimen from patients and controls. We analyzed samples for the presence of MAP specific DNA and to demonstrate humoral response to a MAP protein (MAP2694), a predicted homologue of the T-cell receptor gamma-chain/complement component 1 of the host. We found presence of MAP DNA in 42% of the MS patients and an extremely significant humoral immune response revealed by the MS patients against the MAP protein. In our opinion, this is the first report that significantly associates MAP infection with MS. Further studies will be required to confirm if MAP could be one of the triggers of MS, according to the molecular mimicry theory, in susceptible (and genetically at risk) individuals.
Highlights
Multiple sclerosis (MS) is a chronic, autoimmune and demyelinating syndrome that primarily affects the central nervous system
A total of 21 out of 50 MS patients were observed positive by PCR (42%) based on the amplification of IS900, a specific signature element within the genome of Mycobacterium avium subsp. paratuberculosis (MAP), whereas, only 7 out of 56 samples in the control group were observed positive (12.5%) (Table 1)
A possibly significant epitope was identified and highlighted on the image between amino acids 301–309. It is located within the homology between MAP2964 and T cell receptor gamma chain/complement component 1 of the host and it has a high probability to be exposed on the surface of the membrane
Summary
Multiple sclerosis (MS) is a chronic, autoimmune and demyelinating syndrome that primarily affects the central nervous system. NRAMP1 is an iron transporter associated with macrophage activation This gene has multiple pleiotropic effects on macrophage function, including regulation of cytokine production, tumor necrosis factor a, interleukin-1 b, inducible nitric oxide synthase and regulation of major histocompatibility complex class II expression and antigen presentation functions [7,8]. All of these activities are essential for protection against mycobacterial infection (innate defenses), and critically involved in the induction and progression of autoimmune diseases [5,7,8]
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