Campylobacter sialyltransferase gene polymorphism directs clinical features of Guillain-Barré syndrome.

Progress has been made in Guillain-Barré syndrome, a post-infectious autoimmune neuropathy, especially on identifying Campylobacter jejuni genes responsible for the development and determinant of clinical features. C. jejuni strains carrying a sialyltransferase gene (cst-II), which is essential for the biosynthesis of ganglioside-like lipo-oligosaccharides (LOSs), are associated with the development of Guillain-Barré syndrome. The C. jejuni sialyltransferase (Cst-II) consists of 291 amino acids, and the 51st determines its enzymatic activity. Strains with cst-II (Thr51) expressed GM1-like and GD1a-like LOS, whereas strains with cst-II (Asn51) expressed GT1a-like and GD1c-like LOS. Patients infected with the cst-II (Thr51) strains had anti-GM1 or anti-GD1a IgG antibodies, and showed limb weakness. Patients infected with the cst-II (Asn51) strains had anti-GQ1b IgG antibodies, and showed ophthalmoplegia and ataxia. The cst-II gene is responsible for the development of Guillain-Barré and Fisher syndromes, and the polymorphism (Thr/Asn51) determines which syndrome develops after C. jejuni enteritis.