Helicobacter pylori (H. pylori) causes gastritis and intestinal metaplasia (TM) that may evolve to gastric carcinoma. Paradoxically, IM leads to clearing of H. pylori, except for some cases in which it persists in damaging the mucosa. The objective of this study was to compare the profile of mucins and type 1 Lewis antigens in IM cases with and without H. pylori. Gastric biopsies (n=32) were double-stained using immunohistochemistry (MUC1, MUC2, MUC5AC, MUC6, Le(a), sialyl-Le(a), and Le(b)) and histochemistry for H. pylori. H. pylori was observed in association with IM in 4 of 22 biopsies with IM (complete IM - 6; incomplete IM - 16). The four biopsies with IM and H. pylori displayed a particular pattern of incomplete IM: expression of MUC1 and MUC5AC and little/no expression of MUC2. The 18 biopsies with IM and without H. pylori had high levels of MUC2 expression, regardless of the IM type. The pattern of expression of type 1 Lewis antigens was similar in IM, regardless of the presence or absence of H. pylori. It is concluded that H. pylori is able to colonize incomplete IM whenever it contains foci expressing MUCI and MUC5AC and no MUC2, independently from Le(a), sialyl-Le(a) and Le(b). The results suggest, furthermore, that MUC2 expression affects the ability of H. pylori to colonize IM areas, regardless of the levels of expression of MUC1 and MUC5AC.