Dental Follicle Stem Cells Ameliorate Lipopolysaccharide-Induced Inflammation by Secreting TGF-β3 and TSP-1 to Elicit Macrophage M2 Polarization

摘要: Background/aims Increasing evidence has demonstrated the novel roles of mesenchymal stem cells (MSCs) in immunotherapy. However, difficulty acquiring these and possible ethical issues limited their application. Recently, we have isolated a unique MSC population from dental follicles with potent cell-like properties. This study focused on effects follicle (DFSCs) macrophage activation polarization to determine role immunomodulation test if DFSCs are promising cell source for MSC-based Methods Rat acute lung injury (ALI) models induced by Lipopolysaccharide (LPS) were applied immune-modulatory DFSC/DFSC-CM vivo. The pulmonary permeability was determined dry / wet weight ratios left upper lobe. histopathological damage graded 0 4+ scale. And inflammatory cytokines bronchoalveolar lavage fluid (BALF) tested ELISA. Then established LPS-induced inflamed vitro. Inflammatory cytokine production marker expression measured RT-qPCR, ELISA, western blot flow cytometric analysis macrophages following DFSC-CM treatment. paracrine factors revealed RayBiotech Protein Array. Thereafter, neutralization studies performed confirm potential immune regulators DFSC-CM. Results not only attenuated permeability, but also downregulated pro-inflammatory MCP-1, IL-1, IL-6 TNF-α, upregulated anti-inflammatory IL-10 BALF. Immunofluorescence staining increased M2 Arg-1. Further vitro that switched an phenotype when co-cultured DFSC-CM, characterized suppressed IL-6, TNF-α M1-polarizing markers iNOS CD86; M2-polarizing Arg-1 CD163. A Array 42 differentially expressed (> 2-fold) compared serum-free Ham's F-12K medium, among which TGF-β3 Thrombospondin-1 (TSP-1) 18- 105-fold, respectively. Neutralization confirmed immunoregulatory TSP-1 polarization. Conclusion These results indicated can reprogram into phenotype, may be one underlying mechanisms. supports hypothesis