Compromised autophagy by MIR30B benefits the intracellular survival of Helicobacter pylori
Compromised autophagy by MIR30B benefits the intracellular survival of Helicobacter pylori
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MIR30B 受损的自噬有利于幽门螺杆菌的细胞内存活
DOI：
10.4161/auto.20159
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发表时间：
2012-07-01
期刊：
影响因子：
13.3
通讯作者：
Mao, Xu-Hu
中科院分区：
文献类型：
--
作者：
Tang, Bin;Li, Na;Mao, Xu-Hu
幽门螺杆菌逃避免疫反应，并在胃中实现持续定植。然而，H.幽门螺杆菌感染是否持续尚不清楚。在这项研究中，我们发现MIR30 B在H.幽门螺杆菌感染的AGS细胞系和人胃组织。MIR30 B的上调通过损害H期间的自噬过程而有利于细菌复制。幽门感染作为这一观察结果的潜在机制解释，我们证明MIR30 B直接靶向ATG12和BECN 1，这是参与自噬的重要蛋白质。这些结果表明MIR30 B对自噬的损害允许细胞内H. pylori逃避自噬清除，从而促进H.幽门感染。
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.