ANTI-GM(1) IGG ANTIBODIES AND CAMPYLOBACTER BACTERIA IN GUILLAIN-BARRE-SYNDROME - EVIDENCE OF MOLECULAR MIMICRY

In Guillain-Barre syndrome antibodies to GM(1) and the presence of an antecedent Campylobacter jejuni infection are correlated with a more s evere course of the disease. From a group of 137 consecutive GBS patie nts, 11 sera had elevated titers of anti-GM(1) IgG antibodies during t he acute stage of disease. Each serum sample was preincubated with thr ee different Penner serotypes of whole C. jejuni (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-Barre syndrome patient, inhibi ted 63 to 93% of the anti-GM(1) activity in 6 of 11 patients. The PEN O:41 inhibited 63 to 100% of the anti-GM(1) antibody activity in 9 of 11 patients. The PEN O:22 inhibited anti-GM(1) antibody activity in on ly 2 of 11 patients (80 and 86%). Two Guillain-Barre syndrome patients did not show antibody absorption by any of the Campylobacter serotype s tested, although this does not exclude the involvement of other sero types. An Escherichia coli control strain did not significantly absorb anti-GM(1) antibodies. The results of this study indicate that anti-G M(1) IgG antibodies in Guillain-Barre syndrome sera recognize surface epitopes on whole Campylobacter bacteria and that this recognition is strain-specific. This provides evidence for molecular mimicry in the p athogenesis of Guillain-Barre syndrome.