AIM: To determine if mir-30 d inhibits the autophagy response to Helicobacter pylori(H. pylori) invasion and increases H. pylori intracellular survival.METHODS: The expression of mir-30 d was detected by quantitative polymerase chain reaction(PCR), and autophagy level was examined by transmission electron microscopy, western blot, and GFP-LC3 puncta assay in human AGS cells and GES-1 cells. Luciferase reporter assay was applied to confirm the specificity of mir-30 d regulation on the expression of several core molecules involved in autophagy pathway. The expression of multiple core proteins were analyzed at both the m RNA and protein level, and the intracellular survival of H. pylori after different treatments was detected by gentamicin protection assay.RESULTS: Autophagy level was increased in AGS and GES-1 cells in response to H. pylori infection, which was accompanied by upregulation of mir-30 d expression(P < 0.05, vs no H. pylori infection). In the two gastric epithelial cell lines, mimic mir-30 d was found to repress the autophagy process, whereas mir-30 d inhibitor increased autophagy responseto H. pylori invasion. mir-30 d mimic decreased the luciferase activity of wild type reporter plasmids carrying the 3′ untranslated region(UTR) of all five tested genes(ATG2B, ATG5, ATG12, BECN1, and BNIP3L), whereas it had no effect on the mutant reporter plasmids. These five genes are core genes of autophagy pathway, and their expression was reduced significantly after mir-30 d mimic transfection(P < 0.05, vs control cells without mir-30 d mimic treatment). Mir-30 d mimic transfection and direct inhibition of autophagy increased the intracellular survival of H. pylori in AGS cells.CONCLUSION: Mir-30 d increases intracellular survival of H. pylori in gastric epithelial cells through inhibition of multiple core proteins in the autophagy pathway. AIM: To determine if mir-30 d inhibits the autophagy response to Helicobacter pylori (H. pylori) invasion and increases H. pylori intracellular survival. METHODS: The expression of mir-30 d was detected by quantitative polymerase chain reaction (PCR) and autophagy level was examined by transmission electron microscopy, western blot, and GFP-LC3 puncta assay in human AGS cells and GES-1 cells. Luciferase reporter assay was applied to confirm the specificity of mir-30 d regulation on the expression of several cores molecules involved in autophagy pathway. The expression of multiple core proteins were analyzed at both of the RNA and protein levels, and the intracellular survival of H. pylori after different treatments was detected by gentamicin protection assay .RESULTS: Autophagy level increased in AGS and GES-1 cells in response to H. pylori infection, which was accompanied by upregulation of mir-30 d expression (P <0.05, vs no H. pylori infection). In the two gastric epithelial cell line s, mimic mir-30 d was found to repress the autophagy process, mir-30 d inhibitor increased autophagy response to H. pylori invasion. mir-30 d mimic decreased the luciferase activity of wild type reporter plasmids carried the 3 ’untranslated region UTR) of all five tested genes (ATG2B, ATG5, ATG12, BECN1, and BNIP3L), but it it no effect on the mutant reporter plasmids. These five genes are core genes of autophagy pathway, and their expression was reduced significantly after mir- 30 d mimic transfection (P <0.05 vs control cells without mir-30 d mimic treatment). Mir-30 d mimic transfection and direct inhibition of autophagy increased the intracellular survival of H. pylori in AGS cells. CONCLUSION: Mir-30 d increases intracellular survival of H. pylori in gastric epithelial cells through inhibition of multiple core proteins in the autophagy pathway.