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Evidence of Borrelia autoimmunity-induced component of Lyme carditis and arthritis

Elizabeth S Raveche1, Steven E Schutzer, Helen Fernandes

  • 1Department of Pathology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, 185 S. Orange Ave., Newark, NJ 07103, USA.

Journal of Clinical Microbiology
|February 8, 2005
PubMed

Insights

Lyme disease symptoms like arthritis may stem from molecular mimicry, where Borrelia burgdorferi proteins resemble self-components. This study reveals cross-reactivity, suggesting a link to autoimmunity in susceptible hosts.

Area of Science:

  • Immunology
  • Microbiology
  • Autoimmunity

Background:

  • Lyme disease manifestations like arthritis and carditis may involve autoimmunity.
  • Molecular mimicry, where pathogen components resemble host self-components, is a potential mechanism.

Purpose of the Study:

  • To investigate if Borrelia burgdorferi (B. burgdorferi) proteins mimic self-components, potentially causing autoimmunity.
  • To explore the immunological cross-reactivity between B. burgdorferi and host tissues.

Main Methods:

  • Comparative analysis of amino acid sequences between Streptococcus pyogenes M protein and B. burgdorferi OspA protein.
  • Western blot and ELISA assays using antibodies against S. pyogenes M5 and sera from B. burgdorferi-infected mice.
  • Infection of autoimmune-prone NZB mice and comparison of disease severity and antibody responses with control strains.

Main Results:

  • Significant amino acid homologies were found between S. pyogenes M protein and B. burgdorferi OspA.
  • Antibodies against S. pyogenes M5 and sera from infected mice showed cross-reactivity with myosin and B. burgdorferi proteins.
  • NZB mice infected with B. burgdorferi exhibited exacerbated joint swelling and cross-reactive antibody responses.

Conclusions:

  • B. burgdorferi possesses epitopes that mimic self-proteins, leading to immunological cross-reactivity.
  • This mimicry may contribute to autoimmunity in susceptible individuals or animals infected with Lyme disease.
  • Findings suggest a potential mechanism for autoimmune manifestations in Lyme disease pathogenesis.

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