[Polyradiculoneuritis and Campylobacter jejuni: clinical and physiopathological aspects].

Several explanations have been proposed to explain the relationship between axonal forms of acute auto-immune inflammatory polyradiculoneuritis and Campylobacter jejuni. The major hypothesis involving molecular imitation is based on the existence of common antigenic determinants (epitopes) in the lipopolysaccharides of the infectious agent and gangliosides, i.e. glycosphingolipides on the surface of the nervous system cells, especially peripheral nervous system cells. The purpose of this literature review is to improve understanding of the rather complex physiopathological mechanisms underlying Guillain-Barre syndrome.