Helicobacter pylori from asymptomatic hosts expressing heptoglycan but lacking Lewis O-chains: Lewis blood-group O-chains may play a role in Helicobacter pylori induced pathology

Helicobacter pylori is a widespread Gram-negative bacterium responsible for the onset of various gastric pathologies and cancers in humans. A familiar trait of H. pylori is the production of cell-surface lipopolysaccharides ( LPSs; O-chain right arrow core right arrow lipid A) with O-chain structures analogous to some mammalian histo-blood-group antigens, those being the Le wis determinants (Le(a), Le(b), Le(x), sialyl Le(x), Le(y)) and blood group s A and linear B. Some of these LPS antigens have been implicated as autoim mune, adhesion, and colonization components of H. pylori pathogenic mechani sms. This article describes the chemical structures of LPSs from H. pylori isolated from subjects with no overt signs of disease. Experimental data fr om chemical- and spectroscopic-based studies unanimously showed that these H. pylori manufactured extended heptoglycans composed of 2- and 3-linked D- glycero-alpha-D-manno-heptopyranose units and did not express any blood-gro up O-antigen chains. The fact that another H. pylori isolate with a similar LPS structure was shown to be capable of colonizing mice indicates that H. pylori histo-blood-group structures are not an absolute prerequisite for c olonization in the murine model also. The absence of O-chains with histo-bl ood groups may cause H. pylori to become inept in exciting an immune respon se. Additionally, the presence of elongated heptoglycans may impede exposur e of disease-causing outer-membrane antigens. These factors may render such H. pylori incapable of creating exogenous contacts essential for pathogene sis of severe gastroduodenal diseases and suggest that histo-blood groups i n the LPS may indeed play a role in inducing a more severe H. pylori pathol ogy.