Bacterial infections in Guillain-Barre and Fisher syndromes
Bacterial infections in Guillain-Barre and Fisher syndromes
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DOI：
10.1097/01.wco.0000245367.36576.e9
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发表时间：
2006-10-01
影响因子：
4.8
通讯作者：
Koga, Michiaki
中科院分区：
文献类型：
--
作者：
Yuki, Nobuhiro;Koga, Michiaki
综述目的对格林-巴利综合征的认识已取得进展，尤其是在鉴定与临床特征发生有关的空肠弯曲菌基因方面。最近的研究结果根据脂寡糖生物合成基因的组织将空肠弯曲菌分为几类。一类携带唾液酸转移酶基因(CST-II)的基因与格林-巴利综合征的发生有关，格林-巴利综合征对神经节苷脂低聚糖的生物合成是必不可少的。空肠弯曲菌同时表达类GM1和GD1a样脂低聚糖，可诱导产生抗GM1、抗GD1a或抗GM1/GD1a复合体的自身抗体，可能增加发病风险。空肠弯曲菌唾液酸转移酶(CST-II)由291个氨基酸组成，第51个氨基酸决定其酶活性。携带CST-II(Thr51)的菌株表达类GM1或GD1a样脂低聚糖，而携带CST-II(Asn51)的菌株表达类GT1a或GD1c样脂低聚糖。感染CST-II(Thr51)株的患者有抗GM1或抗GD1a抗体，表现为肢体无力。感染CST-II(Asn51)菌株的患者存在抗GO1b抗体，并表现为眼肌麻痹和共济失调。摘要CST-II基因与格林-巴利综合征和Fisher综合征的发生有关，而Thr/Asn51基因的多态性决定了空肠炎后的综合征。
Purpose of review Progress has been made in our understanding of Guillain-Barre syndrome, especially in identifying the Campylobacter jejuni genes responsible for the development of clinical features.Recent findings C. jejuni is grouped into several classes based on the organization of lipo-oligosaccharide biosynthesis genes. A specific class carrying a sialyltransferase gene (cst-II) is associated with the development of Guillain-Barre syndrome, which is essential for the biosynthesis of ganglioside-like lipo-oligosaccharides. The class of C.jejuni expressed both GM1-like and GD1a-like lipooligosaccharides, which could induce the production of autoantibodies to GM1, to GD1 a or to the GM1/GD1a complex, possibly increasing the risk of development. C. jejuni sialyltransferase (Cst-II) consists of 291 amino acids, and the 51st amino acid determines its enzymatic activity. Strains with cst-II (Thr51) expressed GM1-like or GD1 a-like lipo-oligosaccharide whereas strains with cst-II (Asn51) expressed GT1a-like or GD1 c-like lipooligosaccharide. Patients infected with the cst-II (Thr51) strains had anti-GM1 or anti-GD1 a IgG antibodies, and showed limb weakness. Patients infected with the cst-II (Asn51) strains had anti-GO1b IgG antibodies, and showed ophthalmoplegia and ataxia.Summary 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.