Distinct gene expression profiles in gastric epithelial cells induced by different clinical isolates of Helicobacter pylori--implication of bacteria and host interaction in gastric carcinogenesis.

Background/aims: Helicobacter pylori (H. pylori) infection is a major risk factor of peptic ulcer, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. The interplay between H. pylori and host is an important issue for elucidation of pathogenesis of H. pylori-related diseases. We aimed to examine simultaneously dynamic changes of multiple molecular pathways of infection affected by different H. pylori strains by cDNA microarrays.

Methodology: To elucidate the cross-talk between H. pylori and gastric epithelial cells, we isolated three different H. pylori strains from patients with gastric cancer (GC), duodenal ulcer (DU), and gastric MALT lymphoma (MA). The bacteria were co-cultured with gastric epithelial cells (AGS) and total RNAs were extracted from AGS cells and used for detection of genes represented in the microarray.

Results: Of the 12,814 clones on the microarray, there were 522 genes expressed differently in the three groups. Of the 522 genes, there were 4 genes, 4 genes and 13 genes, either up- or down-regulated more than twofold change, in AGS cells induced specifically by GC, MA, and DU strain, respectively. The GC and DU strains induced more genes involving in carcinogenesis, such as pim-1, jun B, and VEGF.

Conclusions: Our data by cDNA microarray suggest bacterial factors may determine the outcomes of H. pylori infection. The expression profiles of cDNA microarray provide clues for diagnosis, treatment, and prevention of H. pylori-related gastroduodenal diseases.