Compromised autophagy by<i><i>MIR30B</i></i>benefits the intracellular survival of<i><i>Helicobacter pylori</i></i>

Abstract excerpt

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...

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