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

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 mucos a, we evaluated whether the patterns of expression of Le(x) and Le(y) on He licobacter pylori lipopolysaccharides reflected those of host expression of Le(a) and Le(b). When 79 patients (secretors and nonsecretors) were examin ed 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 d ifference between the amount of Le(x) or Le(y) expressed on isolates from u lcer and chronic gastritis patients (P > 0.05). Also, the effect of host an d bacterial expression of Le antigens on bacterial colonization and the obs erved inflammatory response was assessed. In ulcer patients, Le(x) expressi on was significantly related to neutrophil infiltration (r(s) = 0.481, P = 0.024), whereas in chronic gastritis patients significant relationships wer e 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 lym phocyte 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 lymphocy te (r(s) = 0.277, P = 0.029) infiltrates. Thus, although no evidence of con cordance 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 an tigens.