HELICOBACTER-PYLORI INCREASES PROLIFERATION OF GASTRIC EPITHELIAL-CELLS

The direct and indirect effects of Helicobacter pylori on cell kinetic s of gastric epithelial cell line AGS were investigated by flow cytome tric analysis of Ki-67 positive cells and by MTT assay. Flow cytometri c analysis of Ki-67 positivity permits detection of cells that are in S-phase, whereas the MTT assay is a colometric measure of the number o f viable cells. In the absence of added stimulants, 23.06 (4.88)% mean (SD) of AGS cells were Ki-67 positive. When cells were preincubated i n the presence of H pylori, there was a significant increase in Ki-67 positivity (66.20 (7.89)%, p<0.001). This increase was not seen in cel ls cultured in the presence of Campylobacter jejuni (24.63 (8.11)% or Escherichia coli (21.66 (9.78)%). Pre-incubation of AGS cells with sup ernatants from both H pylori and mitogen activated peripheral blood ly mphocytes also increased the per cent of cells that were Ki-67 positiv e (72.93 (8.68) and 69.96 (12.35)%; p,0.001) respectively. Similar res ults were also found in MTT assay. These data show that both H pylori directly and the immune/inflammatory response to H pylori indirectly c an influence the rate of epithelial cell proliferation, suggesting thi s bacterium may be an initiating step in gastric carcinogenesis and an important co-carcinogenic factor in H pylori positive subjects.