Article

Animal models are fundamental to advance knowledge of disease pathogenesis and to
test/develop new therapeutic strategies. Most of the current knowledge about the
pathogenic mechanisms underpinning autoimmune demyelination processes implicating
autoantigens has been obtained using the Experimental Autoimmune Neuritis (EAN)
animal model. The most widely used EAN model is obtained by active immunization
of Lewis rats using a peptide, P0 (180-199), issuing from the major peripheral
nervous system myelin protein. But this model mimics only the classical
monophasic acute form of demyelinating polyradiculoneuropathy, i.e.
Guillain-Barre syndrome (GBS). We developed a new model by immunizing Lewis rats
using the same immunodominant neuritogenic peptide P0 (180-199) but this time
with its S-palmitoyl derivative, S-palm P0 (180-199). All of the animals
immunized with the S-palm P0 (180-199) peptide developed a chronic
relapsing-remitting form of the disease corresponding to the electrophysiological
criteria of demyelination (slow sensory nerve conduction velocity, prolonged
motor nerve latency, partial motor nerve conduction blocks) with axon
degeneration. These findings were confirmed by immunohistopathology study and
thus, appear to mimic human chronic inflammatory demyelinating polyradiculopathy
(CIDP). This new model opens up new avenues of research for testing new
anti-inflammatory and neuroprotective therapeutic strategies.
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Langue : ANGLAIS