Lipopolysaccharides in the development of the Guillain-Barre syndrome and Miller Fisher syndrome forms of acute inflammatory peripheral neuropathies

Guillain-Barre syndrome (GBS), an acute inflammatory polyneuropathy, is pre ceded in most cases by an infectious illness, and Campylobacter jejuni, a l eading cause of acute gastroenteritis, is the most common antecedent to GBS and its ocular variant, Miller Fisher syndrome (MFS). O (Penner) serotypin g is considered to distinguish between C. jejuni strains based on differenc es in lipopolysaccharide (LPS) structure. Serotypes of C. jejuni uncommon i n enteritis, such as serotype O.19 and O:41, have been associated with GBS. Chemical studies on the core oligosaccharide (OS) of C. jejuni LPSs from s erotypes including O:1, O:2, O:4, O:10, O:19, O:23, O:36 and O:41 have reve aled structures that mimic human gangliosides including GM(1), GD(1a), GD(2 ), GD(3), and GM(2). Research has focused on the view that molecular mimicr y may be a factor in the pathogenesis of GBS. Serum antibodies against gang liosides, particularly GM(1) ganglioside, are present in 30% of GBS patient s, and are highly associated with MFS, but are generally absent in enteriti s cases uncomplicated by neuropathy. Collective data from human and animal studies with anti-ganglioside antibodies suggest a pathogenic role for the antibodies. Many aspects of the pathogenesis of GBS are unclear, in particu lar how LPS is presented to T cells or the role of host factors in disease development.