In humans, various peptic diseases and ailments are attributed to infection by the Gram-negative bacterium,
Helicobacter pylori. Among the various pathogenic factors of
H. pylori, the lipopolysaccharides (LPS) display two different characteristics to LPS of other Gram-negative bacteria. These include low biological activity and the presence of structures similar to human blood Lewis antigens. The former is derived from
H. pylori lipid A structure that contains long fatty acids (βOHC
18, βOHC
16 and C
16) and is deficient in the phosphate group at the non-reducing end of glucosamine disaccharide, compared to the lipid A structure of
Escherichia coli. Epitopes similar to the Lewis antigen structure are present in the non-reducing end unit of the
O-polysaccharide moiety, which may lead to the adhesion and colonization of this bacterium with human gastric epithelial cells. Recently, epitopes distinct from Lewis related antigens were identified in the
O-polysaccharide moiety. These novel epitopes appear to be associated with peptic disease.
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