Miller-Fisher syndrome associated with Campylobacter jejuni bearing lipopolysaccharide molecules that mimic human ganglioside GD3

Abstract

Campylobacter jejuni strain of serotype O:10 was isolated from a patient who had Miller-Fisher syndrome. In its biochemical reactions and cellular morphology, the isolate was characteristic of typical C. jejuni. Antibodies against extracted lipopolysaccharide (LPS) were detected by passive hemagglutination in the acuteand convalescent-phase patient sera. By sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting with the O:10 antiserum, it was demonstrated that the strain possessed both low-and highmolecular-weight molecules. Chemical analysis of the LPS revealed that the core oligosaccharide has a terminal trisaccharide epitope consisting of two molecules of sialic acid linked to galactose, a structure reflecting the terminal region of human ganglioside GD 3. As this trisaccharide is also present in LPS cores of serotype O:19 strains from patients with Guillain-Barré syndrome but not in cores of nonneuropathic C. jejuni, a possible role for the trisaccharide in the etiology of neuropathies is indicated, and a difference for distinguishing neuropathic strains from nonneuropathic strains may be the presence of a sialyltransferase required for the synthesis of this trisaccharide.

Brucella melitensisinfection associated with Guillain–Barré syndrome through molecular mimicry of host structures

“…We also noted that immunization with B. melitensis induced the production of anti-GM1 ganglioside antibodies and flaccid limb weakness in BALB/c mice. The development of GBS is thought to result from molecular mimicry between the outer core structures of bacterial lipooligosaccharides and human gangliosides [4], and in this regard, the cores of different isolates of C. jejuni have been shown to mimic GM1, GM2, GD3, GD1a, GT1a and GQ1b [3,4,27,[30][31][32]. The most common antecedent infections of GBS are due to C. jejuni, Mycoplasma pneumoniae, Haemophilus influenzae, Epstein-Barr virus and cytomegalovirus [33][34][35][36][37], and recent studies have suggested a relationship between B. melitensis infection and GBS.…”

The structures of the lipooligosaccharide and capsule polysaccharide of Campylobacter jejuni genome sequenced strain NCTC 11168

“…Proteinase K-treated whole cells of C. jejuni were prepared according to the method of Salloway et al [27] based on the original method of Hitchcock and Brown [28]. The samples were separated on 16.5% deoxycholate-PAGE [29].…”

Role of capsular modified heptose in the virulence of Campylobacter jejuni

“…Survival of C. jejuni within macrophages for several days is also a key virulence factor (Kiehlbauch et al, 1985;Day et al, 2000), and epithelial and macrophage cell damage resulting from invasion may be critical for the inflammatory response elicited by C. jejuni infection (Manninen et al, 1982;Newell and Pearson, 1984;Newell et al, 1985;Fauchere et al, 1986;Szymanski et al, 1995;Biswas et al, 2000). Further, the surface expression of lipooligosaccharide (LOS), which in many C. jejuni strains mimics human gangliosides, has been associated with autoimmune reactions implicated in the Guillain-Barre and Miller Fischer syndromes (Mishu and Blaser, 1993;Yuki et al, 1994;Salloway et al, 1996;Godschalk et al, 2007).…”