Effect of Helicobacter pylori infection on stromal-derived factor-1/CXCR4 axis in bone marrow-derived mesenchymal stem cells.
Effect of Helicobacter pylori infection on stromal-derived factor-1/CXCR4 axis in bone marrow-derived mesenchymal stem cells.
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DOI：
10.4103/2277-9175.124650
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发表时间：
2014
影响因子：
1
通讯作者：
Jalili A
中科院分区：
文献类型：
--
作者：
Fakhari S;Kalantar E;Nikzaban M;Hakhamneshi MS;Fathi F;Nikkhoo B;Rahmani MR;Beiraghdar M;Jalili A
最近的研究表明，在慢性幽门螺杆菌感染过程中，骨髓间充质干细胞（BMD-MSCs）向胃组织迁移，也可能是胃腺癌的起源。趋化因子CXCR4通过与其配体基质衍生因子（SDF-1）的结合，在炎症细胞和干细胞的迁移中起着至关重要的作用。然而，幽门螺杆菌感染对SDF-1/CXCR4轴可能产生的影响尚不清楚。将胃上皮细胞、AGS和BMD-MSCs与幽门螺杆菌共培养24 h，采用定量逆转录聚合酶链反应（qRT-PCR）和流式细胞术检测BMD-MSCs中CXCR4的表达，采用qRT-PCR和酶联免疫吸附法检测AGS细胞中SDF-1的表达。此外，通过趋化性实验评估BMD-MSCs向SDF-1的迁移。我们发现幽门螺杆菌与BMD-MSCs或AGS共培养：(i)增强BMD-MSCs细胞表面CXCR4的表达，（ii）增加AGS细胞分泌SDF-1。我们一致地观察到，与未经处理的细胞相比，经幽门螺杆菌处理的BMD-MSCs向SDF-1梯度迁移的能力更高。我们发现幽门螺杆菌上调BMD-MSCs中CXCR4的表达，并促进其向SDF-1的迁移。本研究首次证明幽门螺杆菌感染可能通过作用于SDF-1/CXCR4轴促进BMD-MSC迁移。
Recent studies have demonstrated that during chronic Helicobacter pylori (H. pylori) infection bone marrow-derived-mesenchymal stem cells (BMD-MSCs) migrate to the gastric tissue and could be also the origin of gastric adenocarcinoma. The chemokine CXCR4 through binding to its ligand stromal-derived factor (SDF-1) plays a crucial role in migration of inflammatory and stem cells. However, the possible effect of H. pylori infection on the SDF-1/CXCR4 axis has not yet been elucidated. Gastric epithelial cell line, AGS, and BMD-MSCs were cocultured with H. pylori for 24 h. The expression of CXCR4 was examined in BMD-MSCs by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and flow cytometry, and SDF-1 expression in AGS cells was detected by qRT-PCR and enzyme-linked immunosorbent assay. Further, migration of BMD-MSCs toward SDF-1 was evaluated by chemotaxis assay. We found that coculture of H. pylori with BMD-MSCs or AGS: (i) enhanced CXCR4 expression on the cell surface of BMD-MSCs and (ii) increased SDF-1 secretion by AGS cells. Consistently, we observed that H. pylori-treated BMD-MSCs showed a higher capability to migrate toward SDF-1 gradient compared with untreated cells. We found that H. pylori upregulates CXCR4 expression in BMD-MSCs and enhance their migration toward SDF-1. This study provides the first evidence that H. pylori infection may enhance BMD-MSC migration through acting on the SDF-1/CXCR4 axis.