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空肠弯曲菌肠炎后吉兰-巴雷综合征和米勒-费雪综合征的发病机制。

Pathogenesis of Guillain-Barré and Miller Fisher syndromes subsequent to Campylobacter jejuni enteritis.

作者信息

Yuki N

机构信息

Department of Neurology, Dokkyo University School of Medicine, Tochigi, Japan.

出版信息

Jpn J Infect Dis. 1999 Jun;52(3):99-105.

Abstract

Some patients developed Guillain-Barré syndrome (GBS) after the administration of bovine gangliosides. Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside. Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside. We showed the existence of molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from patients with GBS, and that between GQ1b and C. jejuni lipopolysaccharides from patients with MFS. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies. This sugar mimicry is one possible cause for GBS and MFS, and unidentified host factor may contribute to the development of these syndromes.

摘要

一些患者在注射牛神经节苷脂后出现了吉兰-巴雷综合征(GBS)。空肠弯曲菌肠炎后发生GBS的患者通常具有抗GM1神经节苷脂的IgG抗体。米勒-费雪综合征(MFS)是GBS的一种变异型,与抗GQ1b神经节苷脂的IgG抗体有关。我们发现,从GBS患者分离出的空肠弯曲菌的GM1与脂多糖之间存在分子模拟,以及从MFS患者分离出的空肠弯曲菌脂多糖与GQ1b之间存在分子模拟。感染因子与神经节苷脂之间的分子模拟可能在抗神经节苷脂抗体的产生中起作用。这种糖类模拟是GBS和MFS的一个可能原因,而不明的宿主因素可能促成这些综合征的发生。

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