Koga M, Takahashi M, Masuda M, Hirata K, Yuki N
Department of Neurology, Dokkyo University School of Medicine, Kitakobayashi 880, Mibu, Shimotsuga, Tochigi 321-0293, Japan.
Neurology. 2005 Nov 8;65(9):1376-81. doi: 10.1212/01.wnl.0000176914.70893.14. Epub 2005 Sep 14.
Ganglioside epitopes on Campylobacter jejuni are hypothesized as the key to the development and characterization of Guillain-Barré syndrome (GBS), but a comprehensive theory has yet to be established. A C jejuni gene, cst-II, involved in the biosynthesis of ganglioside-like lipo-oligosaccharide, shows a polymorphism (Asn/Thr51) that affects ganglioside epitopes.
To examine the hypothesis that this polymorphism determines autoantibody reactivity, and thereby neurologic presentations in GBS.
C jejuni isolates were collected from 105 GBS (including its variants) and 65 uncomplicated enteritis patients. The authors examined the frequency of cst-II and polymorphism (Asn/Thr51) in connection with the bacterial ganglioside epitopes, autoantibody reactivities against GM1, GD1a, and GQ1b, and patients' neurologic findings.
Neuropathic strains more frequently had cst-II, in particular cst-II (Thr51), than did enteritic ones (85% vs 52%; p < 0.001). Strains with cst-II (Asn51) regularly expressed the GQ1b epitope (83%), whereas those with cst-II (Thr51) had the GM1 (92%) and GD1a (91%) epitopes. The presence of these bacterial epitopes in neuropathy patients corresponded to autoantibody reactivity. Patients infected with C jejuni (Asn51) more often were positive for anti-GQ1b IgG (56% vs 8%; p < 0.001) and had ophthalmoparesis (64% vs 13%; p < 0.001) and ataxia (42% vs 11%; p = 0.001). Patients who had C jejuni (Thr51) more frequently were positive for anti-GM1 (88% vs 35%; p < 0.001) and anti-GD1a IgG (52% vs 24%; p = 0.006) and had limb weakness (98% vs 71%; p < 0.001).
The genetic polymorphism of C jejuni determines autoantibody reactivity as well as the clinical presentation of Guillain-Barré syndrome (GBS), possibly through modification of the host-mimicking molecule. The GBS paradigm is the first to explain the detailed pathogenesis of a postinfectious, autoimmune-mediated, molecular mimicry-triggering disorder.
空肠弯曲菌上的神经节苷脂表位被认为是吉兰 - 巴雷综合征（GBS）发生发展及特征表现的关键因素，但尚未建立全面的理论。一个参与类神经节苷脂脂寡糖生物合成的空肠弯曲菌基因cst-II，存在影响神经节苷脂表位的多态性（Asn/Thr51）。
检验这一多态性决定自身抗体反应性，进而决定GBS神经学表现的假说。
从105例GBS（包括其变异型）患者和65例非复杂性肠炎患者中收集空肠弯曲菌分离株。作者研究了cst-II的频率及其多态性（Asn/Thr51）与细菌神经节苷脂表位、针对GM1、GD1a和GQ1b的自身抗体反应性以及患者神经学表现之间的关系。
神经病型菌株比肠炎型菌株更频繁地携带cst-II，尤其是cst-II（Thr51）（85%对52%；p<0.001）。携带cst-II（Asn51）的菌株经常表达GQ1b表位（83%），而携带cst-II（Thr51）的菌株具有GM1（92%）和GD1a（91%）表位。神经病患者中这些细菌表位的存在与自身抗体反应性相对应。感染空肠弯曲菌（Asn51）的患者抗GQ1b IgG阳性更为常见（56%对8%；p<0.001），且有眼肌麻痹（64%对13%；p<0.001）和共济失调（42%对11%；p = 0.001）。感染空肠弯曲菌（Thr51）的患者抗GM1（88%对35%；p<0.001）和抗GD1a IgG阳性更为常见（52%对24%；p = 0.006），且有肢体无力（98%对71%；p<0.001）。
空肠弯曲菌的基因多态性决定自身抗体反应性以及吉兰 - 巴雷综合征（GBS）的临床表现，可能是通过修饰模拟宿主的分子实现的。GBS范例首次解释了一种感染后、自身免疫介导、分子模拟引发疾病的详细发病机制。
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