Editor: Alex van Belkum
Molecular mimicry in Campylobacter jejuni: role of the lipo-oligosaccharide core oligosaccharide in inducing anti-ganglioside antibodies
Article first published online: 21 MAR 2007
FEMS Immunology & Medical Microbiology
Volume 50, Issue 1, pages 27–36, June 2007
How to Cite
Perera, V. N., Nachamkin, I., Ung, H., Patterson, J. H., McConville, M. J., Coloe, P. J. and Fry, B. N. (2007), Molecular mimicry in Campylobacter jejuni: role of the lipo-oligosaccharide core oligosaccharide in inducing anti-ganglioside antibodies. FEMS Immunology & Medical Microbiology, 50: 27–36. doi: 10.1111/j.1574-695X.2007.00225.x
- Issue published online: 21 MAR 2007
- Article first published online: 21 MAR 2007
- Received 22 September 2006, revised 8 December 2006, accepted 11 January 2007.First published online 21 March 2007.
- Campylobacter jejuni;
- Guillain–Barré syndrome;
- waaF gene;
Campylobacter jejuni is recognized as the most common identifiable pathogen associated with the development of Guillain–Barré syndrome (GBS), an acute autoimmune-mediated disease affecting the peripheral nervous system. The immune response to ganglioside-like structures in lipo-oligosaccharides (LOSs) of certain C. jejuni strains is thought to cross-react with human nerve gangliosides and induce GBS. To study the involvement of LOSs in the pathogenesis of Campylobacter-induced GBS, we created truncated LOS molecules by inactivating the waaF gene in a GBS-associated isolate of C. jejuni. Gas Chromatography–MS analysis of the waaF mutant LOSs revealed a marked reduction in sugar content, including sialic acid and galactose. GM1 and GD1a-like mimicry was not detected in the waaF mutant by Western blot analysis with cholera toxin B and anti-GD1a antibodies. Mice immunized with the waaF mutant failed to develop anti-GM1 or anti-GD1a antibodies. The waaF mutant also showed reduced adherence to and invasion of INT-407 cells. The results indicate that the LOS of C. jejuni HB93-13 is essential for adherence and invasion as well as for anti-ganglioside antibody induction.