| Objective: Guillain-Barre syndrome (GBS) is an autoimmune disease of the peripheral nervous system. In the postpolio era, GBS is the most frequent cause of acute flaccid paralysis, occurring with an annual incidence between 1 and 4 per 100 000 people. Acute motor axonal neuropathy (AMAN) is a subtype of GBS. AMAN is encountered in China, Japan and Mexico with a relatively higher frequency. Its clinical feature is impairment of motor function involved respiratory muscle, while sensory function remain intact. Its incidence of disability is high, and prognosis is poor. Pathological changes are Wallerian-like degeneration with rare demyelination and inflammatory cell infiltration. GBS is correlate with many antecedent infections. Many researches suggest that the most frequent infections pathogen linked with GBS is the Gram-negative bacterium Campylocbater jejuni. But its pathogenesis remains ill-defined. People speculated that there is molecular mimicry between Cj and human nerve tissue, ganglioside. It is likely that immune responses directed towards the infecting organisms are involved in the pathogenesis of AMAN by cross-reaction with neural tissues.Experimental autoimmune neuritis (EAN) is widely considered as an animal model of AIDP. EAN can be induced in Lewis rat by immunization with peripheral nervous system myelin or with the P2 protein or P0 protein or synthetic P2 peptides or P2 protein-specific lymphocyte lines. The animal model is very convenient for further scientific research. But there are seldom researches about animal model of AMAN worldwide. Li Chunyan et al made a successful animal model of AMAN. The animal model was induced in chicken by immunization of Cj. However the animal model has many limitations and lower incidence. For this reason, we select two strains of domestic usual experimental rats: Wistar rat and SD rat. The two strains of rat were inoculated with Cj in order to search a rat model of AMAN and explore its pathogenesis.Material and Method: Sixty Wistar rats were divided into two groups: test group and control group. And sixty SD rats similarly were divided into two groups. The first week, each rat of test group were immunized by injection into four footpads and several locations of the back of the body with Freund's complete adjuvant and inactivation antigen of Cj-Pen O:19. 1,2,3,4 weeks after the first immunization, all rats of test group were injected subcutaneously to the back and intraperitoneally with inactivation Cj. All rats of control group were immunized with normal saline. In the course of immunization we observed carefully the clinical symptoms of all rats. The 5th week after the first immunization, blood sample of each rat was taken by eyeball extirpation. Serum sample was collected for further test. Cerebrum, cerebellum, spinal cord and two sides of sciatic nerves and plexus brachialis were dissected as soon as possible after each rat were sacrificed. Bilateral sciatic nerves and plexus brachialis were divided into three segments. One segment was prepared for teased fiber analysis. One segment and Cerebrum, cerebellum, spinal cord were stained with hematoxy-eosin for histopathology assessment. One segment was prepared for electron-macroscopic assessment. The enzyme-linked immunosorbent assay(ELISA) was performed to detect six kinds of antibodies: IgG IgM antibodies of anti-Cj, anti-LPS and anti-GM1 . Result: In test group twenty-one of forty wistar rats immunized with Cj develop a series of clinical symptom. They included progressive weight loss, limp tail and lateral hind legs paresis. Severity of clinical symptom peaked on 15-17 day post immunization. In contrast, Wistar rats of control group and SD rats did not develop any of these signs except weight loss. The incidence of Wistar test group that have clinical symptom was 52.5%. While the incidence of SD group was 0%. There was significant difference between SD test group and Wistar test group (P<0.01). Macroscopic assessment showed typical wallerian-like degeneration in sciatic nerves from thr... |
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