Anti‐GM₁ IgG antibodies and campylobacter bacteria in Guillain‐Barré syndrome: Evidence of molecular mimicry

In Guillain‐Barré syndrome antibodies to GM₁ and the presence of an antecedent Campylobacter jeJunei infection are correlated with a more severe course of the disease. From a group of 137 consecutive GBS patients, 11 sera had elevated titers of anti‐GM₁ IgG antibodies during the acute stage of disease. Each serum sample was preincubated with three different Penner serotypes of whole C. jeJunei (PEN O:4/59, PEN O:41) and Campylobacter coli (PEN O:22) bacteria. The PEN O:4/59 serotype, isolated from the stools of a Guillain‐Barré syndrome patient, inhibited 63 to 93% of the anti‐GM₁ activity in 6 of 11 patients. The PEN O:41 inhibited 63 to 100% of the anti‐GM₁ antibody activity in 9 of 11 patients. The PEN O:22 inhibited anti‐GM₁ antibody activity in only 2 of 11 patients (80 and 86%). Two Guillain‐Barré syndrome patients did not show antibody absorption by any of the Campylobacter serotypes tested, although this does not exclude the involvement of other serotypes. An Escherichia coli control strain did not significantly absorb anti‐GM₁ antibodies. The results of this study indicate that anti‐GM₁ IgG antibodies in Guillain‐Barré syndrome sera recognize surface epitopes on whole Campylobacter bacteria and that this recognition is strain‐specific. This provides evidence for molecular mimicry in the pathogenesis of Guillain‐Barré syndrome.