Helicobacter pylori is a risk factor for gastric cancer, and bacterial-epithelial interactions may be critical in this association. Studies using complementary DNA arrays indicated that the ADAM (A disintegrin and metalloproteinase) genes in gastric epithelial cells are differentially expressed after bacterial-epithelial interactions. Reverse-transcription polymerase chain reaction analysis of gastric biopsy specimens from patients with and without H. pylori showed that infection was associated with increased expression of ADAM 10 and ADAM 17 (tumor necrosis factor-alpha-converting enzyme) in antral mucosa, but no increases in ADAM 15 and ADAM 20 were observed. Increased ADAM 10 transcripts were observed only in cagA-negative infections. High levels of ADAM 10, ADAM 17, and ADAM 20 transcripts were present in gastric carcinoma. H. pylori stimulated temporal changes in ADAM 10 and ADAM 17 transcripts in gastric epithelial cells. Chronic infection with H. pylori may result in persistent mucosal increases in members of the ADAMs family. ADAMs-mediated ectodomain shedding may have a role in gastric carcinogenesis.