Fibronectin (FN) cooperated with TLR2/TLR4 receptor to promote innate immune responses of macrophages via binding to integrin β1
Macrophages could adhere to extracellular matrix molecules(ECM) to induce the expression of pro-inflammatory mediators and phagocytosis that contribute to the pathogenesis of pulmonary infection diseases. Fibronectin (FN) is a large glycoprotein capable of interacting with various ECM molecules prod...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2018-12-01
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| Series: | Virulence |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/21505594.2018.1528841 |
| Summary: | Macrophages could adhere to extracellular matrix molecules(ECM) to induce the expression of pro-inflammatory mediators and phagocytosis that contribute to the pathogenesis of pulmonary infection diseases. Fibronectin (FN) is a large glycoprotein capable of interacting with various ECM molecules produced by a variety of cell types and involved in cell attachment and chemotaxis. However, it is unknown whether FN regulates the expression of pro-inflammatory mediators and phagocytosis of macrophages in the injured lung tissue. Here, we investigated the interaction between FN and integrin β1 in macrophages, which promotes toll-like receptor 2/4 (TLR2/TLR4) signaling pathways to enhance expression of pro-inflammatory mediators and phagocytosis by macrophages. Our results show that lipopolysaccharide (LPS), lipoteichoic acid (LTA) and peptidoglycan (PGN) significantly increase FN expression of macrophages; FN substantially enhances interleukin 6 (IL-6), tumor necrosis factor-α (TNFα), ras-related C3 botulinum toxin substrate 1/2 (Rac1/2), and cell division control protein 42 homolog (Cdc42) expression and phagocytosis of macrophages. However, FN could not enhance pro-inflammatory cytokines and phagocytosis of macrophages induced by LPS and PGN in integrin β1-/- macrophages. Furthermore, applied integrin β1 blocking peptide abrogated the effects that FN promotes innate immune responses of macrophages to LPS and PGN. Those data indicated that the enhanced pro-inflammatory mediators and phagocytosis of macrophages by FN-integrin β1 signal was through co-operating with TLR2/TLR4 signaling. This study suggests that FN play an essential role in the pathogenesis of pulmonary infection disease. |
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| ISSN: | 2150-5594 2150-5608 |