Mycobacterium avium subspecies paratuberculosis and myelin basic protein specific epitopes are highly recognized by

Marco Bo1, Magdalena Niegowska1, Giannina Arru2

  • 1Department of Biomedical Sciences, University of Sassari, Viale San Pietro 43b, 07100 Sassari, Italy.

Insights

Neuromyelitis optica spectrum disorder (NMOSD) patients show higher antibodies to Mycobacterium avium subsp. paratuberculosis (MAP) and myelin basic protein (MBP) than healthy individuals. Unlike in multiple sclerosis (MS), Epstein-Barr virus (EBV) antibody levels were similar in NMOSD patients and controls.

Area of Science:

  • Neuroimmunology
  • Infectious Disease Immunology
  • Autoimmune Disorders

Background:

  • Epstein-Barr virus (EBV) is a known environmental factor linked to neuromyelitis optica spectrum disorder (NMOSD).
  • Studies in multiple sclerosis (MS) suggest cross-reactivity between Mycobacterium avium subsp. paratuberculosis (MAP) peptides and Epstein-Barr virus (EBV)/human epitopes (MBP, IRF5).

Purpose of the Study:

  • To investigate if serological reactivity to MAP and myelin basic protein (MBP) peptides follows a distinct pattern in NMOSD compared to MS and healthy controls.
  • To assess the role of EBV, MAP, and MBP antibodies in NMOSD pathogenesis.

Main Methods:

  • Analysis of serum antibody levels against MAP, MBP, and EBV in 34 NMOSD patients and healthy controls.
  • Comparison of serological findings between NMOSD patients, previously studied MS cohorts, and healthy controls.

Main Results:

  • NMOSD patients exhibited significantly higher levels of antibodies against MAP (44% vs. 5%, p<0.0002) and MBP (50% vs. 2%, p<0.0001) compared to healthy controls.
  • In contrast to MS findings, antibody responsiveness to EBV was comparable between NMOSD patients and healthy controls.
  • These results suggest a specific immune response pattern in NMOSD involving MAP and MBP.

Conclusions:

  • Seroreactivity to MAP and MBP, but not EBV, appears to be a distinguishing feature in NMOSD.
  • The findings support the hypothesis of molecular mimicry involving MAP and MBP in NMOSD pathogenesis.
  • Further research is warranted to elucidate the precise role of these microbial antigens in NMOSD development.

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