Cross-Reactive Antibodies against Gangliosides and Campylobacter jejuni Lipopolysaccharides in Patients with Guillain-Barré or Miller Fisher Syndrome

• Published in: The Journal of infectious diseases Vol. 175; no. 3; pp. 729 - 733
• Main Authors: Jacobs, Bart C., Hazenberg, Maarten P., van Doorn, Pieter A., Endtz, Hubert Ph, van der Meché, Frans G. A.
• Format: Journal Article
• Language: English
• Published: Chicago, IL University of Chicago Press 01.03.1997; Oxford University Press
• Subjects: Antibodies; Antibodies, Bacterial - immunology; Bacteria; Bacterial diseases; Bacterial diseases of the digestive system and abdomen; Biological and medical sciences; Campylobacter jejuni; Campylobacter jejuni - immunology; Cholera Toxin - chemistry; Concise Communications; Cross Reactions; Enteritis; Enzyme linked immunosorbent assay; Epitopes; Gangliosides; Gangliosides - immunology; Human bacterial diseases; Humans; Infections; Infectious diseases; Lipopolysaccharides; Lipopolysaccharides - immunology; Medical sciences; Miller Fisher syndrome; Molecular mimicry; Neuraminidase - chemistry; Neuritis - immunology; Polyradiculoneuropathy - immunology; Polyradiculoneuropathy - microbiology; Campylobacteraceae; Inflammatory disease; Result; Assay; Immunology; Fisher syndrome; Bacteria; Intestinal disease; Evolution; Enteritis; Peripheral nerve disease; Biological effect; Human; Nervous system diseases; Enzyme; Antibody; Campylobacter jejuni; Symptomatology; Concomitant disease; Ganglioside; Glycosidases; Exo-α-sialidase; Digestive diseases; Hydrolases; O-Glycosidases; Guillain Barré syndrome
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/175.3.729

Campylobacter jejuni was isolated from stool specimens of 3 patients with Miller Fisher syndrome (MFS) and 2 patients with Guillain-Barré syndrome (GBS). Anti-GQ1b antibodies in serum from all MFS patients cross-reacted with sialidase-sensitive epitopes in the lipopolysaccharide fraction of C. jejuni from these 3 MFS patients. One GBS patient had anti-GMl antibodies that bound with lipopolysaccharide of C. jejuni from a control patient and from the other GBS patient without antiGMl antibodies. This binding was inhibited by cholera toxin but not by pretreatment with sialidase. The C. jejuni isolate from the GBS patient with serum anti-GMl antibodies did not contain anti-GMl antibody-binding epitopes. Our results strongly support the hypothesis that anti-GQ1b antibodies in MFS patients are induced during the antecedent C jejuni infection. In GBS patients, mechanisms other than molecular mimicry may also be involved in the production of anti-GMl antibodies.