目的：急性感染性多发性神经根炎(GBS)病因尚不清楚，目前认为与感染，尤其与空肠弯曲菌(CJ)感染有关，本文研究CJ感染与神经节苷脂(GM1)损伤的关系，探讨GBS的发病机理。方法：采用酶联免疫吸附试验测定31例GBS患儿(经典型急性感染性多发性神经根炎AIDP 23例，急性运动性轴素神经病AMAN 8例)急性期、恢复期血清和急性期脑脊液CJ-IgG抗体及GM1-IgG、GM1-IgM抗体的变化；并与非GBS神经系统疾病患儿(NGBS组)和10例正常儿童(正常组)对比。结果：AMAN急性期、恢复期血清CJ-IgG抗体水平高于NGBS组(P<0.01)，AIDP急性期血清CJ-IgG高于NGBS组(P<0.01)。AMAN、AIDP急性期脑脊液CJ-IgG高于NGBS组(P<0.01)。GBS急性期、恢复期血清GM1-IgM水平高于NGBS组和正常组(P<0.05)；GM1-IgG高于正常组(P<0.05)，但与NGBS组比较差异无显著性(P>0.05)。GBS组脑脊液GM1-IgM水平高于NGBS组(P<0.05)。CJ-IgG与GM1-IgG、GM1-IgM具有明显的相关性(R=0.722，P=0.05)。结论：空肠弯曲菌感染是GBS发病的重要病因。神经节苷脂GM1的免疫损伤在GBS发病中起重要作用。

OBJECTIVE: The cause of Guillain Barre Syndrome (GBS) is still not clear. Some researchers thought that it was related to infection, especilly Campylobacter jejuni (CJ) infection. This paper aims at studying the relationship between CJ infection and Ganglioside GM 1 injury so as to explore the mechanism of GBS. METHODS: The levels of CJ IgG antibody and the antibodies of ganglioside GM 1 IgG and GM 1 IgM were detected by enzyme linked immunosorbent assay in serum or cerebrospinal fluid of 31 children with GBS. Of the 31 patients, there were 23 cases of acute inflammatory demyelinating polyradiculo neuropathy (AIDP) and 8 cases of acute motor axonal neuropathy (AMAN). Thirty three children with non GBS neurological diseases (NGBS group) and 10 normal children were used as the control groups. RESULTS: The serum CJ IgG levels in both acute and recovery phases in the AMAN group were significantly higher than those of the NGBS group (P< 0.01 ); and the serum anti CJ IgG level in the acute phase in the AIDP group also significantly increased compared with that of the NGBS group (P< 0.01 ). The CJ IgG levels in cerebrospinal fluid in acute phase in the AMAN and AIDP groups were higher than that of the NGBS group (P< 0.01 ). The serum GM 1 IgM levels in both acute and recovery phases in the AMAN and AIDP groups were higher than those of the two control groups (P< 0.05 ). The serum GM 1 IgG level was higher than that of the normal control group, but it did not differ from that of the NGBS group. There were significant differences in the GM 1 IgM level in the cerebrospinal fluid between the GBS group and the NGBS group (P< 0.05 ). CJ IgG was positively correlated to GM 1 IgG and GM 1 IgM (R= 0.722 , P= 0.05 ). CONCLUSIONS: CJ infection may be an important cause of in the development GBS. The immunological injury of ganglioside GM 1 may be related to the pathogenesis of GBS.