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Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice
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Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice

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Cross-reactivity between related sequences found in Acinetobacter sp., Pseudomonas aeruginosa, myelin basic protein

L E Hughes1, P A Smith, S Bonell

  • 1Division of Infection, Immunity and Inflammatory Diseases, King's College London, Waterloo Campus, London, SE1 9NN, UK.

Journal of Neuroimmunology
|November 5, 2003
PubMed

Insights

This study found elevated antibodies to bacterial peptides in multiple sclerosis (MS) patients, suggesting molecular mimicry may contribute to MS pathogenesis. Bacterial infections could play a role in this neurological disease.

Area of Science:

  • Neuroimmunology
  • Microbiology
  • Pathogenesis of Multiple Sclerosis

Background:

  • Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system.
  • The role of infectious agents, particularly bacteria, in MS pathogenesis is an area of ongoing research.
  • Molecular mimicry, where microbial antigens resemble host antigens, is a proposed mechanism for autoimmune diseases like MS.

Purpose of the Study:

  • To investigate the potential role of molecular mimicry between bacterial components and myelin antigens in the pathogenesis of multiple sclerosis.
  • To examine antibody responses to specific bacterial peptide sequences and their cross-reactivity with myelin components in MS patients.

Main Methods:

  • Antibody levels against mimicry peptide sequences from Acinetobacter and Pseudomonas aeruginosa, as well as myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG), were measured in MS patients and controls.
  • Cross-reactivity assays were performed using antisera against MBP and MOG with bacterial peptides.

Main Results:

  • Antibodies to mimicry peptides from Acinetobacter, P. aeruginosa, MBP, and MOG were significantly elevated in MS patients compared to controls (p<0.001 for all).
  • Antisera against MBP (residues 110-124) showed reactivity with Acinetobacter and Pseudomonas peptides.
  • MOG (residues 43-57) antisera reacted with an Acinetobacter peptide.

Conclusions:

  • The findings demonstrate elevated antibody responses to bacterial mimicry peptides in MS patients, suggesting a potential role for bacterial infections in MS pathogenesis.
  • Molecular mimicry is not limited to viral antigens, and bacterial components may trigger autoimmune responses in MS.
  • Further research is warranted to elucidate the precise contribution of these cross-reactive antibodies to the neuropathology of MS.

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