Campylobacter gene polymorphism as a determinant of clinical features of Guillain-Barré syndrome

Neurology. 2005 Nov 8;65(9):1376-81. doi: 10.1212/01.wnl.0000176914.70893.14. Epub 2005 Sep 14.


Background: Ganglioside epitopes on Campylobacter jejuni are hypothesized as the key to the development and characterization of Guillain-Barré syndrome (GBS), but a comprehensive theory has yet to be established. A C jejuni gene, cst-II, involved in the biosynthesis of ganglioside-like lipo-oligosaccharide, shows a polymorphism (Asn/Thr51) that affects ganglioside epitopes.

Objective: To examine the hypothesis that this polymorphism determines autoantibody reactivity, and thereby neurologic presentations in GBS.

Methods: C jejuni isolates were collected from 105 GBS (including its variants) and 65 uncomplicated enteritis patients. The authors examined the frequency of cst-II and polymorphism (Asn/Thr51) in connection with the bacterial ganglioside epitopes, autoantibody reactivities against GM1, GD1a, and GQ1b, and patients' neurologic findings.

Results: Neuropathic strains more frequently had cst-II, in particular cst-II (Thr51), than did enteritic ones (85% vs 52%; p < 0.001). Strains with cst-II (Asn51) regularly expressed the GQ1b epitope (83%), whereas those with cst-II (Thr51) had the GM1 (92%) and GD1a (91%) epitopes. The presence of these bacterial epitopes in neuropathy patients corresponded to autoantibody reactivity. Patients infected with C jejuni (Asn51) more often were positive for anti-GQ1b IgG (56% vs 8%; p < 0.001) and had ophthalmoparesis (64% vs 13%; p < 0.001) and ataxia (42% vs 11%; p = 0.001). Patients who had C jejuni (Thr51) more frequently were positive for anti-GM1 (88% vs 35%; p < 0.001) and anti-GD1a IgG (52% vs 24%; p = 0.006) and had limb weakness (98% vs 71%; p < 0.001).

Conclusions: The genetic polymorphism of C jejuni determines autoantibody reactivity as well as the clinical presentation of Guillain-Barré syndrome (GBS), possibly through modification of the host-mimicking molecule. The GBS paradigm is the first to explain the detailed pathogenesis of a postinfectious, autoimmune-mediated, molecular mimicry-triggering disorder.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Autoantibodies / immunology
  • Campylobacter Infections / complications
  • Campylobacter Infections / immunology*
  • Campylobacter jejuni / genetics*
  • Campylobacter jejuni / immunology*
  • Epitopes / genetics
  • Epitopes / immunology
  • G(M1) Ganglioside / immunology
  • Gangliosides / immunology
  • Gene Expression Regulation, Bacterial / genetics
  • Guillain-Barre Syndrome / immunology*
  • Guillain-Barre Syndrome / microbiology
  • Humans
  • Lipopolysaccharides / biosynthesis
  • Lipopolysaccharides / immunology*
  • Molecular Mimicry / genetics*
  • Mutation / genetics
  • Polymorphism, Genetic / genetics
  • Species Specificity


  • Autoantibodies
  • Epitopes
  • Gangliosides
  • Lipopolysaccharides
  • lipid-linked oligosaccharides
  • G(M1) Ganglioside
  • GQ1b ganglioside