P2-peptide induced experimental allergic neuritis: a model to study axonal degeneration

Abstract

In experimental allergic neuritis (EAN) severity of clincal disease and pathology correlate with the dose of antigen (Hahn et al., Lab Invest 59:115–125, 1988). To avoid axonal membrane contamination of the antigen, EAN was induced with a synthetic peptide, corresponding to residues 53–78 of bovine P₂ myelin protein. Severity of EAN correlated with the dose of peptide in the inoculate. The relationship between demyelination, inflammation and axonal degeneration was studied. Low doses resulted in pure demyelination. Axonal degeneration occurred only with high doses of inflammation. The role of macrophages in producing axonal damage is discussed.