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Exchange of lipooligosaccharide synthesis genes creates potential Guillain-Barre syndrome-inducible strains of Campylobacter jejuni.

ABSTRACT: Human ganglioside-like structures, such as GM1, found on some Campylobacter jejuni strains have been linked to inducing the Guillain-Barré Syndrome (GBS). This study shows that a C. jejuni strain without GM1-like molecules acquired large DNA fragments, including lipooligosaccharide synthesis genes, from a strain expressing GM1-like molecules and consequently transformed into a number of potential GBS-inducible transformants, which exhibited a high degree of genetic and phenotypic diversity.

SUBMITTER: Phongsisay V

PROVIDER: S-EPMC1360302 | biostudies-literature | 2006 Feb

REPOSITORIES: biostudies-literature

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Exchange of lipooligosaccharide synthesis genes creates potential Guillain-Barre syndrome-inducible strains of Campylobacter jejuni.

Phongsisay Vongsavanh V Perera Viraj N VN Fry Benjamin N BN

Infection and immunity 20060201 2

Human ganglioside-like structures, such as GM1, found on some Campylobacter jejuni strains have been linked to inducing the Guillain-Barré Syndrome (GBS). This study shows that a C. jejuni strain without GM1-like molecules acquired large DNA fragments, including lipooligosaccharide synthesis genes, from a strain expressing GM1-like molecules and consequently transformed into a number of potential GBS-inducible transformants, which exhibited a high degree of genetic and phenotypic diversity. ...[more]

PMID: 16428786

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Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain-Barre syndrome.

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2006-01-04 | GSE3967 | GEO

Enhanced, sialoadhesin-dependent uptake of Guillain-Barre syndrome-associated Campylobacter jejuni strains by human macrophages.

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Rapid method for sensitive screening of oligosaccharide epitopes in the lipooligosaccharide from Campylobacter jejuni strains isolated from Guillain-Barre syndrome and Miller Fisher syndrome patients.

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Project description:Campylobacter jejuni causes foodborne gastroenteritis and may trigger acute autoimmune sequelae including Guillain Barré Syndrome. Onset of neuromuscular paralysis is associated with exposure to C. jejuni lipooligosaccharide (LOS) classes A, B, C, D, and E that mimic and evoke antibodies against gangliosides on myelin and axons of peripheral nerves. Family members managing a Michigan dairy operation reported recurring C. jejuni gastroenteritis. Because dairy cattle are known to shed C. jejuni, we hypothesized that calves in the sick pen were the source of human infections. Fecal samples obtained from twenty-five calves, one dog, and one asymptomatic family member were cultured for Campylobacter. C. jejuni isolates were obtained from thirteen calves and the family member: C. coli from two calves, and C. hyointestinalis from two calves. Some calves had diarrhea; most were clinically normal. Typing of lipooligosaccharide biosynthetic loci showed that eight calf C. jejuni isolates fell into classes A, B, and C. Two calf isolates and the human isolate possessed LOS class E, associated mainly with enteric disease and rarely with Guillain Barré Syndrome. Multi-locus sequence typing, porA and flaA typing, and whole genome comparisons of the thirteen C. jejuni isolates indicated that the three LOS class E strains that included the human isolate were closely related, indicating zoonotic transmission. Whole-genome comparisons revealed that isolates differed in virulence gene content, particularly in loci encoding biosynthesis of surface structures. Family members experienced diarrheal illness repeatedly over 2 years, yet none experienced GBS despite exposure to calves carrying invasive C. jejuni with LOS known to elicit antiganglioside autoantibodies.

| S-EPMC9112162 | biostudies-literature

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