Guillain-Barré syndrome and Fisher's syndrome following Campylobacter jejuni infection,

Autor(es): Yuki N.; Miyatake T.

Resumo: 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.

Imprenta: Annals of the New York Academy of Sciences, v. 845, p. 330-340, 1998

Identificador do objeto digital: 10.1111/j.1749-6632.1998.tb09685.x

Descritores: Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Cytopathology ; Guillain-Barre Syndrome - Molecular Structure ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Antibodies ; Guillain-Barre Syndrome - Molecular screening ; Guillain-Barre Syndrome - Immunology

Data de publicação: 1998