Su1660 Interleukin-1ß and Tumor Necrosis Factor-α Polymorphisms As Iron Deficiency Risk Markers in Helicobacter Pylori-Infected Children

Introduction: Transactivation of the EGFR involves a triple membrane passing signal (TMPS) via ADAM17 and HB-EGF in gastric epithelial cells is of relevance to gastric carcinogenesis.H. pylori-induced ADAM17 transcript levels are significantly inhibited by EGCG, a natural product from green tea, in MKN-28 human gastric epithelial cells.The aim of this study was to investigate if H. pylori-induced HB-EGF in MKN-28 gastric epithelial cells and H. pylori-induced Adam17 and Hb-egf in immortalized mouse gastric epithelial cells (MGEC) were inhibited by EGCG.Methods: After optimal co-culture time with H. pylori (NCTC11637, cag PAI + ) at 12 hrs was identified, MKN-28 or MGEC gastric epithelial cells were pre-incubated for 1 hr with EGCG (1-100 μM) (concentrations which did not affect bacterial or cell viability) before co-culture with H. pylori.At 12 hrs post-infection when maximum expression of HB-EGF, Adam17 and Hb-egf was evident, RNA was extracted form both cells and evaluated by Northern blotting.Results: HB-EGF transcript levels in MKN-28 cells were significantly reduced (p<0.05,n=3) by EGCG compared to untreated H. pylori controls at a concentration of 100 μM EGCG at 12 hrs post-infection.EGCG (50 μM) significantly inhibited (p<0.05,n = 3) H. pylori-induced Adam17 and Hb-egf transcripts in MGEC cells at 12 hrs postinfection.Conclusions: H. pylori-induced HB-EGF in MKN-28 cells and Adam17 with Hbegf in MGEC cells are significantly inhibited by EGCG.Green tea consumption as an inhibitor for H. pylori-induced gastric cancer, via the TMPS pathway, might have a role in prevention of gastric carcinogenesis.