A BACTERIUM LIPOPOLYSACCHARIDE THAT ELICITS GUILLAIN-BARRE-SYNDROME HAS A GM1 GANGLIOSIDE-LIKE STRUCTURE

There is a strong association between Guillain-Barre syndrome (GBS) an d Penner's serotype 19 (PEN 19) of Campylobacter jejuni. Sera from pat ients with GBS after C jejuni infection have autoantibodies to GM1 gan glioside in the acute phase of the illness. Our previous work has sugg ested that GBS results from an immune response to cross-reactive antig en between lipopolysaccharide (LPS) of the Gram-negative bacterium and membrane components of peripheral nerves. To clarify the pathogenesis of GBS, we have investigated whether GM1-oligosaccharide structure is present in the LPS of C jejuni (PEN 19) that was isolated from a GBS patient. After extraction of the LPS, the LPS showing the binding acti vity of cholera toxin, that specifically recognizes the GM1-oligosacch aride was purified by a silica bead column chromatography. Gas-liquid chromatography-mass spectrometric analysis has shown that the purified LPS contained Gal, GalNAc, and NeuAc, which are sugar components of G M1 ganglioside. H-1 NMR methods [Carr-Purcell-Meiboom-Gill (CPMG), tot al correlation spectroscopy (TOCSY), and nuclear Overhauser effect spe ctroscopy (NOESY)] have revealed that the oligosaccharide structure [G albeta1-3GalNAcbeta1-4(NeuAcalpha2-3)Galbeta] protrude from the LPS co re. This terminal structure [Galbeta1-3GalNAcbeta1-4(NeuAcalpha2-3)Gal beta] is identical to the terminal tetrasaccharide of the GM1 ganglios ide. This is the first study to demonstrate the existence of molecular mimicry between nerve tissue and the infectious agent that elicits GB S.