Fibronectin (FN) cooperated with TLR2/TLR4 receptor to promote innate immune responses of macrophages via binding to integrin β1. Issue 1 (31st December 2018)

• Record Type: Journal Article
• Authors: Fei, Dongsheng; Meng, Xianglin; Yu, Wei; Yang, Songlin; Song, Ning; Cao, Yanhui; Jin, Songgen; Dong, Lina; Pan, Shangha; Zhao, Mingyan
• Is Part Of: Virulence. Volume 9:Issue 1(2018)
• Page Start: 1588
• Page End: 1600
• Publication Date: 2018-12-31
• Subjects: Fibronectin (FN) -- integrin β1 -- toll-like receptor -- phagocytosis of macrophages -- innate immunity -- pulmonary infection disease; Virulence (Microbiology) -- Periodicals; Bacterial diseases -- Periodicals; Molecular microbiology -- Periodicals; 579.05
• DOI: 10.1080/21505594.2018.1528841
• Languages: English
• ISSNs: 2150-5608

Abstract

ABSTRACT: 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.