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The role of lipopolysaccharide in Helicobacter pylori pathogenesis.
Author(s) -
Moran AP
Publication year - 1996
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.1996.22164004.x
Subject(s) - helicobacter pylori , pathogenesis , lipopolysaccharide , antigen , immunology , molecular mimicry , mucin , secretion , in vivo , microbiology and biotechnology , gastric mucosa , autoantibody , medicine , biology , antibody , stomach , pathology
The present review describes the structure, attributes and properties of Helicobacter pylori lipopolysaccharides (LPS), and their potential role in pathogenesis. Although possessing certain attributes similar to those of LPS of other Gram‐negative bacteria, H. pylori LPS possess unique biological properties. H. pylori LPS has, in general, low immunological activity and this property may aid the persistence of infection. The O‐specific chain of the LPS mimics Lewis blood group antigens in structure. As these antigens are present in the gastric mucosa, the expression of Lewis antigens on the bacterial surface may camouflage the bacterium and aid survival of H. pylori. Alternatively, since autoantibodies against human antral gastric mucosa have been observed in H. pylori‐positive patients, the relevance of LPS in the development of autoimmunity in H. pylori‐associated disease requires further investigation. H. pylori LPS in part mediates the binding of the bacterium to laminin, and interferes with gastric cell receptor‐ laminin interaction, thereby potentially contributing to the loss of mucosal integrity. In vitro observations of inhibition of sulphated mucin synthesis and stimulation of pepsinogen secretion by LPS suggest new mechanisms for H. pylori‐induced mucosal damage. Nevertheless, further in vivo studies are required to support their pathogenic role.