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

Department of Microbiology, National University of Ireland, Galway, Ireland

Anthony P. Moran

Department of Microbiology, National University of Ireland, Galway, Ireland, anthony.moran{at}nuigalway.ie

Guillain-Barré syndrome (GBS), an acute inflammatory polyneuropathy, is preceded in most cases by an infectious illness, and Campylobacter jejuni, a leading cause of acute gastroenteritis, is the most common antecedent to GBS and its ocular variant, Miller Fisher syndrome (MFS). O (Penner) serotyping is considered to distinguish between C. jejuni strains based on differences in lipopolysaccharide (LPS) structure. Serotypes of C. jejuni uncommon in 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 serotypes including O:1, O:2, O:4, O:10, O:19, O:23, O:36 and O:41 have revealed structures that mimic human gangliosides including GM₁, GD_1a, GD ₂, GD₃, and GM₂. Research has focused on the view that molecular mimicry may be a factor in the pathogenesis of GBS. Serum antibodies against gangliosides, particularly GM₁ ganglioside, are present in 30% of GBS patients, and are highly associated with MFS, but are generally absent in enteritis 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 particular how LPS is presented to T cells or the role of host factors in disease development.

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