H. pylori adherence in health and disease. This .gure illustrates the pro.ciency of H. pylori for adaptive multistep mediated attachment. (A) H. pylori (in green) adherence is mediated by the Leb blood group antigen expressed in glycoproteins (blue chains) in the gastric surface epithelium (the lower surface) (3, 32). H. pylori uses BabA (green Y's) for strong and speci.c recognition of the Leb antigen (4). Most of the sLexbinding isolates also bind the Leb antigen (SabA, in red Y's). (B) During persistent infection and chronic in.ammation (gastritis), H. pylori triggers the host tissue to retailor the gastric mucosal glycosylation patterns to up-regulate the in.ammation-associated sLex antigens (red host, triangles). Then, SabA (red Y structures) performs Selectin-mimicry by binding the sialyl-(di)-Lewis x/a glycosphingolipids, for membrane close at tachment and apposition. (C) At sites of vigorous local in.ammatory response, as illustrated by the recruited activated white blood cell (orange "bleb"), those H. pylori subclones that have lost sLex-binding capacity due to ON/OFF frameshift mutation might have gained local advantage in the prepared escaping of intimate contact with (sialylated) lymphocytes or other defensive cells. Such adaptation of bacterial adherence properties and subsequent in.ammation pressure could be major contributors to the extraordinary chronicity of H. pylori infection in human gastric mucosa.