Insights into Campylobacter jejuni-induced Guillain-Barre syndrome from the Lewis rat model of experimental allergic neuritis

Abstract

Experimental allergic neuritis (EAN) is considered the in vivo model of Guillain-Barre syndrome (GBS) and has been extensively studied in the Lewis rat. Both cellular and humoral components of the immune response are implicated in the inflammatory demyelination of peripheral nerves that characterizes EAN. The recognition of Campylobacter jejuni infection as a frequent antecedent event in GBS, and in particular its association with anti-ganglioside antibodies and a primary axonal neuropathy, has raised many questions about the specific disease mechanisms involved. While C. jejuni can produce an acute motor neuropathy in chickens, confirming the relationship between C. jejuni infection and acute neuropathy, no detailed information is available from this animal model. Insights from experimental studies relating to the effector phase of Lewis rat EAN that may be relevant to C. jejuni- induced GBS are discussed.