Tannic acid prevents macrophage-induced pro-fibrotic response in lung epithelial cells via suppressing TLR4-mediated macrophage polarization
| Autor: | Adithi Kannan, Ramalingam Bethunaickan, Rajaguru Palanichamy, Dhamotharan Pattarayan, Lakshmanan Loganathan, Karthikeyan Muthusamy, Nandhine Rajasekar, Ayyanar Sivanantham, Subbiah Rajasekaran, Santanu Kar Mahapatra |
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| Rok vydání: | 2019 |
| Předmět: |
Lipopolysaccharides
0301 basic medicine MAPK/ERK pathway Epithelial-Mesenchymal Transition THP-1 Cells Immunology Anti-Inflammatory Agents Macrophage polarization Mice 03 medical and health sciences 0302 clinical medicine Fibrosis medicine Animals Humans Receptor Lung Pharmacology Chemistry Mesenchymal stem cell Macrophage Activation medicine.disease Cell biology Toll-Like Receptor 4 RAW 264.7 Cells 030104 developmental biology MD2 A549 Cells 030220 oncology & carcinogenesis TLR4 Signal transduction Tannins |
| Zdroj: | Inflammation Research. 68:1011-1024 |
| ISSN: | 1420-908X 1023-3830 |
| Popis: | Polarized macrophages induce fibrosis through multiple mechanisms, including a process termed epithelial-to-mesenchymal transition (EMT). Mesenchymal cells contribute to the excessive accumulation of fibrous connective tissues, leading to organ failure. This study was aimed to investigate the effect of tannic acid (TA), a natural dietary polyphenol on M1 macrophage-induced EMT and its underlying mechanisms. First, we induced M1 polarization in macrophage cell lines (RAW 264.7 and THP-1). Then, the conditioned-medium (CM) from these polarized macrophages was used to induce EMT in the human adenocarcinomic alveolar epithelial (A549) cells. We also analysed the role of TA on macrophage polarization. We found that TA pre-treated CM did not induce EMT in epithelial cells. Further, TA pre-treated CM showed diminished activation of MAPK in epithelial cells. Subsequently, TA was shown to inhibit LPS-induced M1 polarization in macrophages by directly targeting toll-like receptor 4 (TLR4), thereby repressing LPS binding to TLR4/MD2 complex and subsequent signal transduction. It was concluded that TA prevented M1 macrophage-induced EMT by suppressing the macrophage polarization possibly through inhibiting the formation of LPS-TLR4/MD2 complex and blockage of subsequent downstream signal activation. Further, our findings may provide beneficial information to develop new therapeutic strategies against chronic inflammatory diseases. |
| Databáze: | OpenAIRE |
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