Campylobacter Jejuni Lipopolysaccharide Composition Of The Pathogenic Mechanism Of Peripheral Nerve

Part I Pathogenic Role of Lipopolysaccharide of Campylobacter Jejuni in Allergic Neuropathy Induced by the Bacteria IlObjectivel To explore the pathogenic role of Cl LPS in allergic neuropathy induced by the bacteria. jMethodJ Louies rats were immunized by systemic imniuno-potentiation with Cl LPS and Cl respectively. The animals were sacrificed and sciatic nerves were taken on the day of 14th, 21st, 28th and 35th after immunization. Histological study, including teasing fibers and cross-section for toluidine blue stain, was finished under light microscope and electron microscope. Titers of anti-Cl LPS antibody (IgG and 1gM) in serum of immunized rats were detected by ELISA in series on the day of 0th, 7th., 14th, 21st, 28th and 35th respectively. Histological study for sciatic nerve was also performed on the 7th day after injection with immunized serum perineurally. [ResultsJ (1) There were no differences on the incidence of pathologic fibers of sciatic nerve in the rats after systemic inimuno-potentiation between Cl group (11.0%) and Cl LPS group (10.46%). The pathologic change in both groups could be demonstrated since the 14th day with immunization and the peak incidence were met on the 35th day; The pathologic patterns of abnormal fibers were mostly belonged to axonal degeneration (7.63%, 7.57%) but accompanied by demyelination (2.83%, 3.43%); (2) There were also no difference in the incidence of pathologic fibers between Cl group (65.2%) and Cl LPS group (62.5%) after the perineural injection witrh immunized serum. The pathologic fibers in both groups were also belonged to axonal degeneration (55.6%, 54.4%) mostly and less common to demyelination (9.6%, 8.1%); (3) There were no differences in titers of IgG or 1gM anti-CJ LPS antibody between Cl and Cl LPS groups. The titers of 1gM both groups were reached at the peak level on the 14th day after immunization and gradually decreased to normal range before the 4th week, however the titer of LgG were gradually increased after the 14th day and reached the peak level on the 35th day. The peak values of IgG were lasted till the 5 th week; (4) The process developing an allergic neuropathy induced by Cl and Cl LPS in 3 weeks, was completely consisted with the latent period of GBS after Cl infection and the increasing sera titers of anti-Cl LPS IgG antibody in experimental animals. [Conclusionj (1) Cl LPS is the main pathogenic component of Cl antigen in peripheral neuropathy induced by Cl. The pathogenicity and the pathological course caused by Cl LPS were coincided with that of Cl; (2) Anti-Cl LPS antibodies in serum induced after inimuno-potentiation with Cl and Cl LPS were increased and run at a same level. The ability of Cl LPS to cause immunological injury after the perineural injection was also matched to the Cl. It was well demonstrated that the rising antibody after Cl infection would be mainly related to its LPS component.