Contribution of bacterial sialylation in the development of postinfectious autoimmune peripheral neuropathy

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Guillain-Barre syndrome (GBS) is an autoimmune-mediated peripheral neuropathy and most GBS patients have infectious symptoms 1-3 weeks before neurological onset. Campylobacter jejuni, a leading cause of acute enteritis in developed countries, is the most frequent antecedent infectious agent in GBS. Gangliosides (glycosphingolipids with sialic acids) have been identified as a target molecule of GBS after C. jejuni enteritis. In this study, previous these findings lead to examine whether high sialic acid modification ability of C. jejuni is a risk factor for development of GBS. Disappointedly, there was no difference in sialic acid content between the GBS and enteritis (as control) isolates. This was the same when only the strains with ganglioside epitopes or GBS-related LOS biosynthesis locus were analyzed. These results suggest that the quality of the sialylation is more important than the quantity for the development of this syndrome.