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

Abstract

In experimental allergic neuritis (EAN) severity of clinical 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 antigen and in association with very active mononuclear inflammation. The role of macrophages in producing axonal damage is discussed.

• Authors: A F Hahn, T E Feasby, L Wilkie, D Lovgren
• Journal: Acta neuropathologica (Acta Neuropathol) Vol. 82 Issue 1 Pg. 60-5 ( 1991) ISSN: 0001-6322 [Print] Germany
• PMID: 1719739 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Myelin Basic Protein
• Myelin P2 Protein
• Peptide Fragments

Topics

• Animals
• Axons (physiology, ultrastructure)
• Dose-Response Relationship, Drug
• Electrophysiology (methods)
• Ganglia, Spinal (pathology, physiopathology)
• Male
• Myelin Basic Protein (toxicity)
• Myelin P2 Protein
• Neuritis, Autoimmune, Experimental (pathology, physiopathology)
• Peptide Fragments (toxicity)
• Rats
• Rats, Inbred Lew
• Reference Values
• Sciatic Nerve (pathology, physiopathology)
• Spinal Cord (pathology, physiopathology)