Guillain-Barre' syndrome (GBS) is an immune-mediated, inflammatory, demyelinating polyneuropathy. In serum of GBS patients, complement fixing antibodies against peripheral nerve myelin can be found, which correlate with the clinical course and precede the appearance of activated complement components in CSF, serum and peripheral nerve. A significant portion of this Ab activity in some GBS patients is directed against a neutral glycolipid of peripheral nerve myelin that cross-reacts with Forssman antigen. Forssman is a component of several viruses and bacteria, and heterophile responses accompanying many infections are partly directed against Forssman antigen. In this proposal we want to study the role of antibody and complement in peripheral nerve demyelination in experimental allergic neuritis (EAN), an animal model of GBS.
Our specific aims are: 1) To study the development of experimental allergic neuritis in the Lewis rat, following immunization with Forssman antigen. 2) To determine which epitope on Forssman is recognized by serum Ab from Forssman induced EAN animals. 3) To determine if affinity-purified Ab from EAN serum can cause demyelination following intraneural injection in Lewis rat sciatic nerve. 4) To study the effect of complement depletion on blood-nerve barrier integrity in EAN induced by peripheral nerve myelin. Electrophysiologic testing and histologic studies will be done to assess peripheral nerve demyelination in EAN, and after intraneural injection. Immunological techniques to be used include ELISA, C1 fixation-transfer assay and HPTLC.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Clinical Investigator Award (CIA) (K08)
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University of Texas Health Science Center Houston
Schools of Medicine
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