Guillain-Barré syndrome serum and anti-Campylobacter antibody do not exacerbate experimental autoimmune neuritis

J Neuroimmunol. 2001 Oct 1;119(2):306-16. doi: 10.1016/s0165-5728(01)00390-3.

Abstract

To investigate whether antibodies are pathogenic in Guillain-Barré syndrome (GBS), we injected pre-treatment serum from 11 GBS patients intraperitoneally into rats in which the blood-nerve barrier had been opened by induction of mild adoptive transfer experimental autoimmune neuritis. There was no significant clinical, neurophysiological or pathological difference between rats receiving GBS serum compared with those receiving control serum, except that GBS serum caused minor excess weight loss. Murine monoclonal antibody to Campylobacter jejuni and gangliosides also did not exacerbate disease. This experiment failed to show antibody-mediated disease exacerbation and so does not support an antibody-mediated mechanism in GBS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Bacterial / blood
  • Antibodies, Bacterial / immunology
  • Antibodies, Monoclonal
  • Campylobacter / immunology*
  • Campylobacter Infections / immunology*
  • Cauda Equina / immunology
  • Demyelinating Diseases / immunology
  • Female
  • G(M1) Ganglioside / immunology
  • Guillain-Barre Syndrome / immunology*
  • Guillain-Barre Syndrome / microbiology
  • Guillain-Barre Syndrome / pathology
  • Humans
  • Immunization, Passive
  • Immunoglobulin G / blood
  • Immunoglobulin G / immunology
  • Immunoglobulin M / blood
  • Immunoglobulin M / immunology
  • Neural Conduction / immunology
  • Neuritis, Autoimmune, Experimental / immunology*
  • Neuritis, Autoimmune, Experimental / pathology
  • Rats
  • Rats, Inbred Lew
  • Reproducibility of Results
  • Severity of Illness Index
  • Spinal Nerve Roots / immunology
  • Spinal Nerve Roots / pathology
  • Weight Loss

Substances

  • Antibodies, Bacterial
  • Antibodies, Monoclonal
  • Immunoglobulin G
  • Immunoglobulin M
  • G(M1) Ganglioside