Abstract
The patients with Guillain-Barré Syndrome (GBS) subsequent to Campylobacter jejuni enteritis showed axonal degeneration and had IgG anti-GM1 antibody. The most frequently isolated C. jejuni from the patients was specific serotype of Penner's 19 in Japan. In the lipopolysaccharide (LPS) in C. jejuni of this serotype, the same oligosaccharide structure as GM1 ganglioside existed, suggesting the molecular mimicry between GM1 in nervous tissue and C. jejuni LPS. IgG anti-GM1 antibody may bind the nodes of Ranvier and axon terminals and causes degeneration of the motor axon. Some patients develop Fisher's syndrome following C. jejuni infection. C. jejuni strains from the patients who had IgG anti-GQ1b antibody in the acute phase had GQ1b epitope in their LPS, and the molecular mimicry between GQ1b in nervous tissue and an antecedent infectious agent was clarified.
Publication types
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Case Reports
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Autoantibodies / blood*
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Axons / pathology
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Campylobacter Infections / complications*
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Campylobacter Infections / immunology
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Campylobacter jejuni* / immunology
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Campylobacter jejuni* / isolation & purification
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Carbohydrate Sequence
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G(M1) Ganglioside / chemistry
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G(M1) Ganglioside / immunology*
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Gangliosides / immunology
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Humans
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Immunoglobulin G / blood
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Lipopolysaccharides / chemistry
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Lipopolysaccharides / isolation & purification
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Male
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Miller Fisher Syndrome / etiology
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Miller Fisher Syndrome / immunology*
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Miller Fisher Syndrome / physiopathology
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Molecular Sequence Data
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Motor Neurons / pathology
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Oligosaccharides / chemistry
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Polyradiculoneuropathy / etiology
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Polyradiculoneuropathy / immunology*
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Polyradiculoneuropathy / physiopathology
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Ranvier's Nodes / pathology
Substances
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Autoantibodies
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Gangliosides
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Immunoglobulin G
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Lipopolysaccharides
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Oligosaccharides
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G(M1) Ganglioside
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GQ1b ganglioside