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Molecular mechanism of Guillain-Barre syndrome after Campylobacter jejuni enteritis : approach from bacterial analysis

空肠弯曲菌肠炎后格林-巴利综合征的分子机制：细菌分析方法

基本信息

批准号：
16390254
负责人：
YUKI Nobuhiro
金额：
$ 6.66万
依托单位：
Dokkyo Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

项目摘要

Guillain-Barre syndrome (GBS), a post-infectious autoimmune-mediated neuropathy, is a serious complication after Campylobacter jejuni enteritis. To investigate the bacterial risk factor for developing GBS, genotypes, serotypes and ganglioside-mimics on lipo-oligosaccharide (LOS) were analyzed in the isolates from Japanese patients. GBS isolates more frequently were grouped in LOS biosynthesis locus class A (72/106 ; 68%) than were enteritis isolates (17/103 ; 17%). Class A strains predominantly had genotype cst-II (Thr51), which is responsible for biosynthesis of GM1- and GD1a-like LOSs. Indeed we found that strains with cst-II (Thr51) regularly expressed the GM1 and GD1a epitopes, whereas those with cst-II (Asn51) had the GQ1b epitope. Patients who had C.jejuni (Thr51) more frequently were positive for anti-GM1 and anti-GD1a IgG and had limb weakness. Patients infected with C.jejuni (Asn51) more often were positive for anti-GQ1b IgG and had ophthalmoparesis and ataxia. Predominant cst-II genotype was Thr51 in the isolates from GBS patients, whereas it was Asn51 in those with Fisher syndrome. Class A locus clustering in GBS isolates, recently reported in Europe, provides the first GBS-related C.jejuni characteristic common to Asia and Europe. Class A locus seems to be linked to cst-II polymorphism, resulting in promotion of both GM1- and GD1a-like structure synthesis on LOS ; consequently, increasing the risk of producing anti-ganglioside antibodies and developing GBS. The genetic polymorphism of C.jejuni determines autoantibody reactivity and the clinical presentation of GBS, possibly through modification of the host-mimicking molecule.

格林-巴利综合征（GBS）是一种感染后自身免疫介导的神经病，是空肠弯曲菌肠炎后的严重并发症。为了调查形成 GBS 的细菌危险因素，对日本患者分离株的基因型、血清型和脂寡糖 (LOS) 神经节苷脂模拟物进行了分析。 GBS 分离株比肠炎分离株 (17/103; 17%) 更频繁地归入 LOS 生物合成基因座 A 类 (72/106; 68%)。 A 类菌株主要具有基因型 cst-II (Thr51)，该基因型负责 GM1 和 GD1a 样 LOS 的生物合成。事实上，我们发现具有 cst-II (Thr51) 的菌株定期表达 GM1 和 GD1a 表位，而具有 cst-II (Asn51) 的菌株则具有 GQ1b 表位。空肠弯曲菌 (Thr51) 感染频率较高的患者抗 GM1 和抗 GD1a IgG 呈阳性，且有肢体无力。感染空肠弯曲菌 (Asn51) 的患者更常出现抗 GQ1b IgG 阳性，并出现眼肌麻痹和共济失调。 GBS 患者分离株中的主要 cst-II 基因型为 Thr51，而费舍尔综合征分离株中的主要 cst-II 基因型为 Asn51。最近在欧洲报道的 GBS 分离株中的 A 类基因座聚类提供了亚洲和欧洲共有的第一个与 GBS 相关的空肠弯曲菌特征。 A 类基因座似乎与 cst-II 多态性相关，从而促进 LOS 上的 GM1 和 GD1a 样结构合成；因此，增加产生抗神经节苷脂抗体和发展 GBS 的风险。空肠弯曲菌的遗传多态性可能通过模拟宿主分子的修饰来决定自身抗体反应性和 GBS 的临床表现。

项目成果

期刊论文数量（84）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Clinical correlates of serum anti-GT1a IgG antibodies

DOI：
10.1016/j.jns.2004.01.005
发表时间：
2004-04-15
期刊：
JOURNAL OF THE NEUROLOGICAL SCIENCES
影响因子：
4.4
作者：
Nagashima, T;Koga, M;Yuki, N
通讯作者：
Yuki, N

Axonal Guillain-Barre syndrome subtypes : do we need more splitting?

轴突格林-巴利综合征亚型：我们需要更多分裂吗？

DOI：
发表时间：
2003
期刊：
Neurology 61
影响因子：
0
作者：
Hirai M;Suzuki S;Hinokio Y;Yamada T;et al.;Yuki N.
通讯作者：
Yuki N.

Side effects of combined therapy of methylprednisolone and intravenous immunoglobulin in Guillain-Barre syndrome.

甲基强的松龙和静脉注射免疫球蛋白联合治疗吉兰-巴利综合征的副作用。

DOI：
发表时间：
2005
期刊：
Eur Neurol 53
影响因子：
0
作者：
Oohashi T;Bekku Y;Houliston RS;Van Sorge NM;Van Sorge NM;Overell J;Koga M;Kamitani T;Tatsumoto M;Nagasawa K;Houliston RS;Yoshida T;Funakoshi K;Tatsumoto M;Komagamine T;Gono T;Yuki N;Kimoto K;Comin R;Koga M;Koga M;Koga M;Pandey JP;Yuki N;Li J;Yuki N;Odaka M;Odaka M
通讯作者：
Odaka M

Ambiguous value of Haemophilus influenzae isolation in Guillain-Barre and Fisher syndromes