Relationship of blood group determinants on Helicobacter pylori lipopolysaccharide with host lewis phenotype and inflammatory response

Abstract

As Lewis a (Le(a)) and Lewis b (Le(b)) blood group antigens are isoforms of Lewis x (Le(x)) and Lewis y (Le(y)) and are expressed in the gastric mucosa, we evaluated whether the patterns of expression of Le(x) and Le(y) on Helicobacter pylori lipopolysaccharides reflected those of host expression of Le(a) and Le(b). When 79 patients (secretors and nonsecretors) were examined for concordance between bacterial and host Le expression, no association was found (chi(2) = 5.734, 3 df, P = 0.125), nor was there a significant difference between the amount of Le(x) or Le(y) expressed on isolates from ulcer and chronic gastritis patients (P > 0.05). Also, the effect of host and bacterial expression of Le antigens on bacterial colonization and the observed inflammatory response was assessed. In ulcer patients, Le(x) expression was significantly related to neutrophil infiltration (r(s) = 0.481, P = 0.024), whereas in chronic gastritis patients significant relationships were found between Le(x) expression and H. pylori colonization density (r(s) = 0.296, P = 0.03), neutrophil infiltrate (r(s) = 0.409, P = 0. 001), and lymphocyte infiltrate (r(s) = 0.389, P = 0.002). Furthermore, bacterial Le(y) expression was related to neutrophil (r(s) = 0.271, P = 0.033) and lymphocyte (r(s) = 0.277, P = 0.029) infiltrates. Thus, although no evidence of concordance was found between bacterial and host expression of Le determinants, these antigens may be crucial for bacterial colonization, and the ensuing inflammatory response appears, at least in part, to be influenced by Le antigens.

FIG. 1

Correlation between expression of Le^x and Le^y blood group antigens on the LPSs of H. pylori isolated from patients with ulcers (A) and those with chronic gastritis (B). ODU, OD units.