Vriesendorp F J
Department of Neurology, University of Texas Health Science Center, Houston 77030, USA.
J Infect Dis. 1997 Dec;176 Suppl 2:S164-8. doi: 10.1086/513787.
Experimental allergic neuritis (EAN) is considered the in vivo model of Guillain-Barré syndrome (GBS) and has been extensively studied in the Lewis rat. Both cellular and humoral components of the immune response are implicated in the inflammatory demyelination of peripheral nerves that characterizes EAN. The recognition of Campylobacter jejuni infection as a frequent antecedent event in GBS, and in particular its association with anti-ganglioside antibodies and a primary axonal neuropathy, has raised many questions about the specific disease mechanisms involved. While C. jejuni can produce an acute motor neuropathy in chickens, confirming the relationship between C. jejuni infection and acute neuropathy, no detailed information is available from this animal model. Insights from experimental studies relating to the effector phase of Lewis rat EAN that may be relevant to C. jejuni-induced GBS are discussed.
实验性变应性神经炎（EAN）被认为是吉兰-巴雷综合征（GBS）的体内模型，并且已经在Lewis大鼠中进行了广泛研究。免疫反应的细胞和体液成分均与EAN特征性的周围神经炎性脱髓鞘有关。空肠弯曲菌感染被认为是GBS中常见的前驱事件，尤其是它与抗神经节苷脂抗体及原发性轴索性神经病的关联，引发了许多关于所涉及的具体疾病机制的问题。虽然空肠弯曲菌可在鸡中引起急性运动性神经病，证实了空肠弯曲菌感染与急性神经病之间的关系，但该动物模型未提供详细信息。本文讨论了与Lewis大鼠EAN效应期相关的实验研究见解，这些见解可能与空肠弯曲菌诱导的GBS有关。
