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Compromised autophagy by MIR30B benefits the intracellular survival of Helicobacter pylori.

ABSTRACT: Helicobacter pylori evade immune responses and achieve persistent colonization in the stomach. However, the mechanism by which H. pylori infections persist is not clear. In this study, we showed that MIR30B is upregulated during H. pylori infection of an AGS cell line and human gastric tissues. Upregulation of MIR30B benefited bacterial replication by compromising the process of autophagy during the H. pylori infection. As a potential mechanistic explanation for this observation, we demonstrate that MIR30B directly targets ATG12 and BECN1, which are important proteins involved in autophagy. These results suggest that compromise of autophagy by MIR30B allows intracellular H. pylori to evade autophagic clearance, thereby contributing to the persistence of H. pylori infections.

SUBMITTER: Tang B

PROVIDER: S-EPMC3429542 | biostudies-literature | 2012 Jul

REPOSITORIES: biostudies-literature

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Compromised autophagy by MIR30B benefits the intracellular survival of Helicobacter pylori.

Tang Bin B Li Na N Gu Jiang J Zhuang Yuan Y Li Qian Q Wang Hai-Guang HG Fang Yao Y Yu Bo B Zhang Jin-Yu JY Xie Qing-Hua QH Chen Li L Jiang Xue-Jun XJ Xiao Bin B Zou Quan-Ming QM Mao Xu-Hu XH

Autophagy 20120531 7

Helicobacter pylori evade immune responses and achieve persistent colonization in the stomach. However, the mechanism by which H. pylori infections persist is not clear. In this study, we showed that MIR30B is upregulated during H. pylori infection of an AGS cell line and human gastric tissues. Upregulation of MIR30B benefited bacterial replication by compromising the process of autophagy during the H. pylori infection. As a potential mechanistic explanation for this observation, we demonstrate ...[more]

PMID: 22647547

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