Effect of Helicobacter pylori infection on stromal-derived factor-1/CXCR4 axis in bone marrow-derived mesenchymal stem cells
نویسندگان
1 Department of Microbiology, Faculty of Medicine, Alborz University of Medical Sciences, Karaj, Iran
2 Kurdistan Molecular & Cellular Research Center, Kurdistan University of Medical Sciences, Sanadaj, Iran
3 Kurdistan Molecular & Cellular Research Center, Kurdistan University of Medical Sciences, Sanadaj, Iran
4 Kurdistan Molecular & Cellular Research Center, Kurdistan University of Medical Sciences, Sanadaj, Iran
5 Kurdistan Molecular & Cellular Research Center, Kurdistan University of Medical Sciences, Sanadaj, Iran
6 Kurdistan Molecular & Cellular Research Center, Kurdistan University of Medical Sciences, Sanadaj, Iran
7 Kurdistan Molecular & Cellular Research Center, Kurdistan University of Medical Sciences, Sanadaj, Iran
8 Department of Physiology, Isfahan Payamnoor University, Isfahan, Iran
9 Kurdistan Molecular & Cellular Research Center, Kurdistan University of Medical Sciences, Sanadaj, Iran
doi
چکیده
Background: 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 receptor 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.Materials and Methods: 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.Results: 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.Conclusion: 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-MSCs migration through acting on the SDF-1/CXCR4 axis.
