Yuki N, Miyatake T
Department of Neurology, Dokkyo University School of Medicine, Tochigi, Japan.
Ann N Y Acad Sci. 1998 Jun 19;845:330-40. doi: 10.1111/j.1749-6632.1998.tb09685.x.
The patients with Guillain-Barré Syndrome (GBS) subsequent to Campylobacter jejuni enteritis showed axonal degeneration and had IgG anti-GM1 antibody. The most frequently isolated C. jejuni from the patients was specific serotype of Penner's 19 in Japan. In the lipopolysaccharide (LPS) in C. jejuni of this serotype, the same oligosaccharide structure as GM1 ganglioside existed, suggesting the molecular mimicry between GM1 in nervous tissue and C. jejuni LPS. IgG anti-GM1 antibody may bind the nodes of Ranvier and axon terminals and causes degeneration of the motor axon. Some patients develop Fisher's syndrome following C. jejuni infection. C. jejuni strains from the patients who had IgG anti-GQ1b antibody in the acute phase had GQ1b epitope in their LPS, and the molecular mimicry between GQ1b in nervous tissue and an antecedent infectious agent was clarified.
空肠弯曲菌肠炎后发生吉兰-巴雷综合征(GBS)的患者表现出轴突变性,并具有IgG抗GM1抗体。在日本,从这些患者中最常分离出的空肠弯曲菌是彭纳19型的特定血清型。在该血清型空肠弯曲菌的脂多糖(LPS)中,存在与GM1神经节苷脂相同的寡糖结构,这表明神经组织中的GM1与空肠弯曲菌LPS之间存在分子模拟。IgG抗GM1抗体可能会结合郎飞结和轴突终末,并导致运动轴突变性。一些患者在空肠弯曲菌感染后会发展为费舍尔综合征。急性期具有IgG抗GQ1b抗体的患者所分离出的空肠弯曲菌菌株,其LPS中具有GQ1b表位,并且阐明了神经组织中的GQ1b与先前感染因子之间的分子模拟。