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目的 探讨体液免疫及细胞免疫在空肠弯曲菌 (Cj)诱发的周围神经轴索变性 (AMAN)和脱髓鞘 (AIDP)两种病理改变类型在格林 巴利综合征 (Guillain Barresyndrome ,GBS)发生机制中的地位和作用。方法 用灭活Cj Pen19血清型菌株免疫 40只Wistar大鼠 ,经病理学检查证实 2 4只大鼠的 2 4条神经发生周围神经病变 ,包括轴索变性 (11条 )、髓鞘脱失 (4条 )和混合病变 (9条 )。采用免疫组化的方法观察不同病变神经区域免疫物质的沉积并进行超微结构定位 ,同时运用原位杂交技术检测相应病变神经中细胞因子mRNA的表达情况。结果 (1)免疫组化检测结果 :Cj Pen19诱发轴索变性的坐骨神经中 ,免疫物质主要沉积于轴膜 ,IgG、C3d、IgM的阳性率分别为 10 0 %、5 5 %和 0 % ,而髓鞘脱失神经中 ,免疫物质则沉积于髓鞘表面 ,IgG、C3d、IgM的阳性率分别为 5 0 %、2 5 %和 0 % ;(2 )原位杂交结果显示 :轴索变性神经中 ,表达IL 4、IL 5、IL 10及IFN γmRNA的细胞阳性率分别为 6 4%、36 %、45 %和 0 % ;髓鞘脱失神经中其阳性率则分别为 2 5 %、0 %、2 5 %和 75 %。结论 空肠弯曲菌感染诱发周围神经轴索变性及髓鞘脱失的发生机制不同 :轴索变性主要由IgG为主的体液免疫因素介导 ;而在髓鞘脱失的发生过程中 ,细胞免疫则起着非常
Objective To investigate the mechanism of humoral and cellular immunity in the pathogenesis of Guillain Barre syndrome (GBS) induced by Campylobacter jejuni (AMAN) and demyelination (AIDP) In the status and role. Methods Twenty-four Wistar rats were immunized with inactivated Cj Pen19 serotypes, and 24 neuropathies including 24 degenerative axons were identified by pathological examination, including axonal degeneration (11), demyelination 4) and mixed lesions (9). Immunohistochemical method was used to observe the deposition of immunologic substances in different pathological nerve regions and the ultrastructural localization. Meanwhile, the expression of cytokine mRNA in the corresponding lesion nerves was detected by in situ hybridization. Results (1) Immunohistochemical results: In the sciatic nerve of Cj Pen19-induced axonal degeneration, the immunogenic substances mainly deposited on the axial membrane. The positive rates of IgG, C3d and IgM were 100%, 55% and 0%, respectively Immunosuppressants were deposited on the surface of myelin sheath in the demyelination of the myelin sheath. The positive rates of IgG, C3d and IgM were 50%, 25% and 0%, respectively. (2) In situ hybridization showed that the axonal degeneration nerve , The positive rates of IL-4, IL-5, IL-10 and IFN-γmRNA were 64%, 36%, 45% and 0%, respectively. The positive rates of myelin denervation were 25% %, 25% and 75%. Conclusions The pathogenesis of Campylobacter jejuni-induced peripheral axon degeneration and myelin degeneration are different. Axonal degeneration is mainly mediated by humoral immune-mediated factors of IgG. In the process of demyelination, cellular immunity Very playful