The sialic acid residue is a crucial component of C. jejuni lipooligosaccharide ganglioside mimicry in the induction Guillain–Barré syndrome

Abstract

Guillain–Barré syndrome (GBS) is an autoimmune neuropathy that often follows C. jejuni infection. Sialic acid ( N-acetylneuraminic acid, NANA) is a common constituent of lipooligosaccharide (LOS). The molecular mimicry between C. jejuni LOS and human peripheral nerve gangliosides is believed to play an important role in the pathogenesis of GBS. The neuB1 encodes NANA synthetase, required for the synthesis of NANA of C. jejuni LOS. A neuB1 mutant was constructed from a C. jejuni HS:19 wild strain. Mutant LOS could not bind the cholera toxin B subunit, failed to induce anti-GM1 antibodies, and did not cause pathological changes in the peripheral nerves. These data suggest that the NANA residue in LOS is a crucial epitope in realization of ganglioside molecular mimicry.