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目的探索空肠弯曲菌(Campylobactejejuni,CJ)致外周神经损伤的关键结构,为CJ感染相关格林巴利综合征的分子模拟理论提供动物实验证据。方法将32只豚鼠随机分为亲代株组(10只)、变异株组(10只)、对照组(6只)、PBS组(6只),分别用亲代株及弗氏佐剂、galE变异株及弗氏佐剂、PBS及弗氏佐剂、单纯PBS进行全身免疫;动态检测血清细胞壁脂寡糖(LOS)IgG及神经节苷脂GM1IgG抗体水平;检查坐骨神经病理改变,包括单纤维分离、半薄切片光镜及电镜检查。结果①免疫后变异株组及亲代株组LOSIgG抗体水平均明显增高,两组间差异无统计学意义;②免疫后14、28d,亲代株组GM1IgG抗体滴度(0.661±0.290,0.984±0.025)明显高于变异株组(0.193±0.078,0.180±0.063),差异均有统计学意义;③变异株组坐骨神经单纤维病变率4.9%(98/2000),明显低于亲代株组(16%,320/2000),差异有统计学意义,后者主要为轴索变性;④亲代株组半薄切片显示以轴索变性为特征的病理改变;变异株组仅见极少数异常,两组间差异有统计学意义;⑤电镜检查证实光镜所见。结论与亲代株相比,galE变异株缺失神经节苷脂GM1样表位,不能诱导动物产生GM1抗体及周围神经损伤,支持CJ感染后格林巴利综合征发生的分子模拟理论。
Objective To explore the key structure of peripheral nerve injury induced by Campylobactejejuni (CJ) and provide animal experimental evidence for the molecular simulation of Cg-related Guillain-Barre syndrome. Methods Thirty-two guinea pigs were randomly divided into parental group (10), mutant group (10), control group (6), PBS group (6) Strain and Freund’s adjuvant, PBS and Freund’s adjuvant, PBS alone were used for systemic immunization. Serum cell wall lipopolysaccharide (LOS) IgG and ganglioside GM1 IgG antibody were detected dynamically. Pathological changes of sciatic nerve including single fiber, Semi-thin section light microscope and electron microscopy. Results ① After immunization, the levels of LOSIgG antibody in the mutant group and the parental strain group were significantly increased, with no significant difference between the two groups. ② At 14 and 28 days after immunization, the antibody titer of GM1 IgG in the parental strain group was 0.661 ± 0.290,0.984 ± 0.025, (0.193 ± 0.078,0.180 ± 0.063), the differences were statistically significant; ③The single fiber disease rate of sciatic nerve in mutant group was 4.9% (98/2000), which was significantly lower than that in parental group (16% 320/2000), the difference was statistically significant, the latter mainly axonal degeneration; ④ semi-thin section of the parental group showed axonal degeneration characterized pathological changes; mutation group only a very small number of abnormalities, the difference between the two groups have Statistical significance; ⑤ electron microscopy confirmed the light seen. CONCLUSION: GalE mutants lacking ganglioside GM1-like epitopes can not induce GM1 antibody and peripheral nerve injury in animals and support the molecular simulation theory of Guillain-Barre syndrome after CJ infection.