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Anti‐GM 1 IgG antibodies and campylobacter bacteria in Guillain‐Barré syndrome: Evidence of molecular mimicry
Author(s) -
Oomes Peter G.,
Jacobs Bart C.,
Hazenberg Maarten P. H.,
Bänffer John R. J.,
van der Meché Frans G. A.
Publication year - 1995
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410380208
Subject(s) - campylobacter jejuni , molecular mimicry , antibody , guillain barre syndrome , serotype , microbiology and biotechnology , campylobacter , pathogenesis , epitope , bacteria , immunology , virology , medicine , biology , genetics
In Guillain‐Barré syndrome antibodies to GM 1 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‐GM 1 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‐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 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‐GM 1 antibodies. The results of this study indicate that anti‐GM 1 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.