脂磷壁酸
细胞生物学
生物
吞噬作用
TLR2型
整合素
先天免疫系统
纤维连接蛋白
TLR4型
肿瘤坏死因子α
巨噬细胞
信号转导
Toll样受体
CD14型
受体
微生物学
免疫系统
免疫学
细胞外基质
生物化学
体外
细菌
遗传学
金黄色葡萄球菌
作者
Dongsheng Fei,Xianglin Meng,Wei Yu,Shi Yu Yang,Ning Song,Yuan Cao,Songgen Jin,Liang Dong,Shangha Pan,Mingyan Zhao
出处
期刊:Virulence
[Informa]
日期:2018-10-13
卷期号:9 (1): 1588-1600
被引量:21
标识
DOI:10.1080/21505594.2018.1528841
摘要
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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