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Campylobacter sialyltransferase gene polymorphism directs clinical features of Guillain-Barre syndrome Yuki NJ Neurochem 2007[Nov]; 103 Suppl 1 (ä): 150-8Progress has been made in Guillain-Barre 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-Barre 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-Barre and Fisher syndromes, and the polymorphism (Thr/Asn51) determines which syndrome develops after C. jejuni enteritis.|*Polymorphism, Genetic[MESH]|Animals[MESH]|Asparagine/genetics[MESH]|Bacterial Proteins/biosynthesis/*genetics[MESH]|Campylobacter jejuni/*genetics[MESH]|Guillain-Barre Syndrome/genetics/*microbiology[MESH]|Humans[MESH]|Sialyltransferases/*genetics[MESH]|Threonine/genetics[MESH] |
