Effect of Helicobacter pylori infection on stromal-derived factor-1/CXCR4 axis in bone marrow-derived mesenchymal stem cells | Zendy

Ali Jalili | Zendy; Shohreh Fakhari | Zendy; Enayatollah Kalantar | Zendy; Mehrnoush Nikzaban | Zendy; MohammadSaid Hakhamneshi | Zendy; Fardin Fathi | Zendy; Bahram Nikkhoo | Zendy; MohammadReza Rahmani | Zendy; Mina Beiraghdar | Zendy

Open Access

Effect of Helicobacter pylori infection on stromal-derived factor-1/CXCR4 axis in bone marrow-derived mesenchymal stem cells

Author(s) -

Ali Jalili,

Shohreh Fakhari,

Enayatollah Kalantar,

Mehrnoush Nikzaban,

MohammadSaid Hakhamneshi,

Fardin Fathi,

Bahram Nikkhoo,

MohammadReza Rahmani,

Mina Beiraghdar

Publication year - 2014

Publication title -

advanced biomedical research

Language(s) - English

Resource type - Journals

ISSN - 2277-9175

DOI - 10.4103/2277-9175.124650

Subject(s) - mesenchymal stem cell , cxcr4 , stromal cell , bone marrow , chemokine , flow cytometry , cancer research , helicobacter pylori , medicine , stromal cell derived factor 1 , stem cell , immunology , biology , inflammation , pathology , microbiology and biotechnology

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

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