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

格林-巴利综合征（Guillain-Barre syndrome，GBS）是一种自身免疫介导的周围神经病，大多数GBS患者在发病前1-3周有感染症状。空肠弯曲菌是发达国家急性肠炎的主要病因，也是GBS最常见的前驱感染因子。神经节苷脂（含唾液酸的鞘糖脂）是继C.空肠肠炎在本研究中，先前的这些发现导致检查是否高唾液酸修饰能力的C。空肠是发生GBS的危险因素。令人失望的是，GBS和肠炎（作为对照）分离株之间的唾液酸含量没有差异。当仅分析具有神经节苷脂表位或GBS相关LOS生物合成位点的菌株时，这是相同的。这些结果表明，唾液酸化的质量比数量更重要的发展这种综合征。

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.