摘要
目的 探讨空肠弯曲菌毒素致周围神经损伤的作用机理。方法 (1)将PEN 19 CJ毒素 (CJT)免疫后的Wistar大鼠血清 ,以及体外激活的该鼠PBMC上清液 ,分别注入健康大鼠神经外膜下及静脉内。 (2 )取大鼠坐骨神经进行单纤维分离 ,甲苯胺蓝光镜和电镜超微组织病理学检测。 (3)用SABC及FITC 免疫荧光法对与CJT共同作用后的正常大鼠和人坐骨神经 ,以及CJT致病变神经组织标本进行免疫酶组织化学和免疫荧光检测 ,并以核酸杂交技术检测其TNF αmRNA表达。结果 (1)CJT经外膜下及静脉注射均可诱发坐骨神经明显轴索变性及髓鞘脱失病理学改变。外膜下注射组原纤维病变率为 76 8% (2 76 3/ 36 0 0 ) ,对照组仅为 9 6 % (2 30 / 2 4 0 0 ) (P <0 0 1)。静脉注射后病变原纤维发生率于第 3天达高峰 ,为 19 5 % (390 / 2 0 0 0 ) ,持续至第 14天时病变仍为 15 5 % (310 / 20 0 0 ) ,而对照组始终无病变发生 (P <0 0 1)。CJT免疫血清及其PBMC上清液外膜下注射原纤维病变率与对照组无明显差异 (P >0 0 5 )。 (2 )CJT与正常大鼠和人坐骨神经共同孵育后 ,以及CJT致周围神经病变组织免疫化学检测显示不同程度的CJT结合阳性反应。 (3)CJT静脉注射后 ,在周围神经已出现明显病变时 ,其他脏器未见明显组织学异常。结论 (1)
Objective To explore the pathogenesis of the damage to peripheral nerves induced by Campylobacter jejuni exotoxin (CJT). Methods (1) Animal models : ① The CJT was extracted from PEN 19-CJ and injected perineurally and intravenously to Wistar rats. ② The sera and the supernatants of peripheral blood mononuclear cells (PBMCs), taken from the rats immunized with the CJT, were injected perineurally at sciatic nerves of experimental rats and intravenously, respectively. (2) Histopathologic study of sciatic nerves: the animals were sacrificed and their sciatic nerves were examined for tease fibers, transverse section with toluidine blues staining and electron microscopy. (3) Immunohistochemistry: sections of sciatic nerves of either normal rats or human which were incubated with CJT and the sciatic nerves with pathological changes induced by CJT were obtained for observation of the binding capability of CJT with peripheral nerves by SABC and FITC-immunofluorescence methods, and nucleic acid hybridization techniques for detection of TNF-α mRNA expression in pathological sciatic nerves samples. Results (1) Remarkable peripheral neuropathies with axon degeneration and/or demyelination were found in the nerves induced by both CJT injection perineurally and intravenously. The axon degeneration was more obvious. Pathological changes were identified in 76.8% (2 763/3 600) of teasing fibers after perineural injection, but only 9.6% (230/2 400) of fibers were damaged in control group ( P <0.01). The peak severity of fiber damage was found on the 3rd day after CJT intravenous injection with the incidence of abnormal fibers was 19.5% (390/2 000), and abnormalities of 15.5% (310/2000) on the 14th day. However, no abnormal changes were demonstrated in control group ( P <0.01). So was in thegroups injected with anti-CJT sera and the supernatants of PBMCs compared with control ( P >0.05). (2) Binding of CJT to the nerve was found dominant in the sciatic nerves taken from normal rats or human either incubated with CJT or in the
出处
《中华儿科杂志》
CAS
CSCD
北大核心
2003年第12期934-939,共6页
Chinese Journal of Pediatrics
基金
国家自然科学基金资助项目 (3 9770 783 )
