Campylobacter coli enteritis and Guillain-Barre syndrome:: No evidence of molecular mimicry and serological relationship
Campylobacter coli enteritis and Guillain-Barre syndrome:: No evidence of molecular mimicry and serological relationship
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DOI：
10.1016/j.jns.2006.02.010
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发表时间：
2006-07-15
影响因子：
4.4
通讯作者：
Yuki, Nobuhiro
中科院分区：
文献类型：
--
作者：
Funakoshi, Kei;Koga, Michiaki;Yuki, Nobuhiro
从两名具有抗GM 1和抗GD 1 IgG抗体的格林-巴利综合征（GBS）患者中分离出大肠弯曲杆菌。虽然这种细菌和空肠弯曲菌是肠道疾病的常见原因，以前的研究只集中在空肠弯曲菌作为GBS的病原体。为了确定大肠杆菌是否也是一种致病因子，我们研究了这样一种假设，即抗神经节苷脂抗体的产生是由细菌脂寡糖（LOS）上的神经节苷脂模拟物诱导的，就像在空肠弯曲菌相关的GBS中一样。两株大肠杆菌的LOS与抗GM 1和抗CiD 1a IgG单克隆抗体的反应性很弱，而一些GBS相关的大肠杆菌LOS与抗GM 1和抗CiD 1a IgG单克隆抗体的反应性很弱。空肠分离物具有较强的反应性。抗-GM 1和抗-GD 1a IgG抗体从两个病人没有吸收尽可能多的由他们的分离株的LOS是GBS相关的空肠弯曲菌菌株。这些发现不支持神经节苷脂模拟大肠杆菌分离株的LOS的假设。接下来，我们使用细菌外膜蛋白作为抗原，对74名GBS患者、26名Fisher综合征（FS）患者、49名其他神经系统疾病（OND）患者和37名正常对照（NC）患者进行了近期大肠杆菌感染的血清学检测。8例（11%）GBS和2例（8%）FS患者有两种或三种IgG、IgM和伊加抗C。coli抗体。抗C空肠IgG和伊加抗体滴度显著高于抗C.大肠杆菌（分别为p=0.03和0.01）。这表明抗C。coli抗体与C.空肠蛋白我们得出结论，C.大肠杆菌感染不是GBS的病因。从GBS患者中分离出微生物和感染性血清学阳性并不总是指示致病因子。(c)2006 Elsevier B. V.保留所有权利。
Campylobacter coli was isolated from two Guillain-Barre syndrome (GBS) patients who had anti-GM1 and anti-GD1 IgG antibodies. Although both this bacteria and Campylobacter jejuni are common causes of diarrheal illness, previous studies have focused only on C jejuni as the causal agent of GBS. To determine whether C coli also is a causative agent, we examined the hypothesis that production of anti-ganglioside antibodies is induced by ganglioside-mimics on that bacterial lipo-oligosaccharide (LOS), as in C jejuni-associated GBS. LOSs of both C coli isolates had very weak reactivities with anti-GM1 and anti-CiD1a IgG monoclonal antibodies, whereas those of some GBS-related C. jejuni isolates had strong reactivities. Anti-GM1 and anti-GD1a IgG antibodies from the two patients were not absorbed as much by the LOSs of their isolates as were those of GBS-related C jejuni strains. These findings do not support the hypothesis of ganglioside mimicry on C coli isolates' LOSs. We next made a serological assay of recent C coli infection in 74 patients with GBS, 26 with Fisher syndrome (FS), 49 with other neurological diseases (OND), and 37 normal controls (NC) using the bacterial outer membrane protein as antigen. Eight (11%) GBS and two (8%) FS patients had two or three classes of IgG, IgM, and IgA anti-C. coli antibodies. Anti-C. jejuni IgG and IgA antibody titers were significantly higher than those of anti-C. coli (respectively, p=0.03 and 0.01). This suggests that anti-C. coli antibodies cross-react with C. jejuni protein. We concluded that a C. coli infection was not the cause of GBS in our patients. Both isolation of a microorganism from, and the positive infectious serology of, GBS patients do not always indicate the causal agent. (c) 2006 Elsevier B.V. All rights reserved.