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目的探讨空肠弯曲菌(CJ)脂多糖(LPS)中唾液酸(SA)基团参与CJ诱发周围神经病关键性抗原成分的重要地位,为CJLPS与神经节苷脂间的分子模拟推论确立免疫病理学证据。方法构建唾液酸合成酶基因1(neuB1)失活、LPS外核寡糖缺乏SA基团的GBS相关CJO:19变异株。分别以野生株和变异株LPS全身免疫豚鼠,ELISA法检测免疫血清中抗CJLPS和抗神经节苷脂GM1IgG抗体,取坐骨神经作病理学检查。再将免疫血清行坐骨神经外膜下注射并作病理学检查。结果(1)PenO:19CJ变异株的neuB1失活、LPS中SA基团缺失;(2)野生株LPS和变异株LPS全身免疫后,豚鼠均产生高滴度抗LPS特异性IgG;(3)全身免疫后第21、35天,野生株LPS免疫血清中检测到抗GM1IgG抗体,而变异株LPS免疫血清中却测不到该抗体;(4)野生株LPS组中有17.3%的坐骨神经原纤维发生以轴索变性为主(占65.0%)的免疫性损伤,与变异株LPS组比较差异有统计学意义(χ2=125,P<0.01)。而变异株LPS组病变率仅2.4%,与对照组比较差异没有统计学意义(P>0.05);(5)野生株LPS免疫血清神经外膜下注射后,67.8%的豚鼠坐骨神经原纤维发生以轴索变性为主(占68.0%)的病变,而变异株LPS免疫血清注射后仅3.2%的神经原纤维发生病变,差异具有统计学意义(P<0.01)。结论外核寡糖缺乏SA基团的GBS相关CJO:19变异株LPS不再能使实验动物血清中产生高滴度的抗GM1抗体,同时丧失对周围神经的免疫致病力,表明含SA基团的LPS寡糖侧链,是CJ诱发周围神经病的GM1样关键性抗原,从免疫病理学角度证实有关CJ诱发GBS的分子模拟推论。
Objective To investigate the important role of sialic acid (SA) groups in CJ lipopolysaccharide (LPS) in CJ-induced key antigenic components of peripheral neuropathy and to establish immunopathology for the molecular modeling of CJLPS and gangliosides evidence. Methods Construction of GBS-related CJO: 19 mutant with inactivation of sialyl-synthase gene 1 (neuB1) and LPS exopolysaccharide-deficient SA group. Guinea pigs were immunized with wild strain and mutant LPS respectively, anti-CJLPS and anti-ganglioside GM1 IgG antibodies in immune serum were detected by ELISA, and sciatic nerve was taken for pathological examination. Then the immune serum line sciatic nerve subarachnoid injection and for pathological examination. Results (1) Inactivation of neuB1 in PenO: 19CJ mutant and deletion of SA group in LPS; (2) High titer anti-LPS specific IgG was produced in guinea pigs after wild-type LPS and LPS immunization; (3) Antibody against GM1 IgG was detected in the wild-type LPS sera 21 and 35 days after immunization, but not in the LPS-immunized sera. (4) 17.3% of the sciatic nerve fibroblasts The majority of axonal degeneration (65.0%) occurred in autoimmune lesions, which was significantly different from that in LPS group (χ2 = 125, P <0.01). However, the mutation rate of LPS group was only 2.4%, which was not significantly different from the control group (P> 0.05). (5) 67.8% of guinea pig sciatic nerve fibroblasts Axial degeneration was the predominant lesion (68.0%), while only 3.2% neurofibrillary lesions were found in the LPS-immunized sera. The difference was statistically significant (P <0.01). CONCLUSIONS: LPS, a GBS-associated CJO: 19 variant with a LOH-deficient GBS associated with an exosomal ribosomal oligosaccharide, can no longer produce high-titer anti-GM1 antibodies in the serum of experimental animals and also lose the immunogenicity to peripheral nerves. The LPS oligosaccharide side chain is a GM1-like key antigen of CJ-induced peripheral neuropathy. The molecular modeling of CJ-induced GBS is confirmed by immunopathology.