Yuki Nobuhiro
Brain and Mind Centre, the University of Sydney.
Brain Nerve. 2015 Nov;67(11):1341-6. doi: 10.11477/mf.1416200304.
One-thirds of patients develop Guillain-Barré syndrome subsequent to Campylobacter jejuni enteritis. Molecular mimicry exists between C. jejuni lipo-oligosaccharides and human peripheral nerve gangliosides GM1 and GD1a. IgG antibodies against GM1 or GD1a are produced in one out of 5,000 patients with C. jejuni enteritis. The autoantibodies bind to gangliosides at the nodes of Ranvier in the peripheral motor nerves and activate complement in situ. This is followed by the disappearance of the voltage-gated sodium channel clusters at the nodes and disruption of axo-glial junctions at the paranodes. This results in the development of motor nerve conduction failure and muscle weakness in the four limbs.
三分之一的患者在空肠弯曲菌肠炎后会发展为吉兰-巴雷综合征。空肠弯曲菌脂寡糖与人外周神经神经节苷脂GM1和GD1a之间存在分子模拟。每5000例空肠弯曲菌肠炎患者中就有1例产生针对GM1或GD1a的IgG抗体。这些自身抗体与外周运动神经郎飞结处的神经节苷脂结合，并在局部激活补体。随后，郎飞结处电压门控钠通道簇消失，结旁轴突-神经胶质连接破坏。这导致运动神经传导障碍和四肢肌肉无力。
