Expression of mucins (MUC1, MUC2, MUC5AC, and MUC6) and type 1 Lewis antigens in cases with and without Helicobacter pylori colonization in metaplastic glands of the human stomach

Helicobacter pylori ( H. pylori ) causes gastritis and intestinal metaplasia (IM) 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 MUC1 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. Copyright © 2002 John Wiley & Sons, Ltd.