TY - JOUR AU - Xie, Chenxi AU - Fan, Yanyun AU - Huang, Yinshi AU - Wu, Shuangting AU - Xu, Haimei AU - Liu, Lupeng AU - Hu, Yiqun AU - Huang, Qingwen AU - Shi, Huaxiu AU - Wang, Lin AU - Xu, Hongzhi AU - Su, Jingling AU - Ren, Jianlin PY - 2020 TI - Class A1 scavenger receptors mediated macrophages in impaired intestinal barrier of inflammatory bowel disease JF - Annals of Translational Medicine; Vol 8, No 4 (February 29, 2020): Annals of Translational Medicine (Focus on "Intrauterine Adhesion") Y2 - 2020 KW - N2 - Background: This study was to investigate the cytokines and phenotype of macrophages pre-treated with class A1 scavenger receptor (SR-A1) antibody in vitro and the influence on apoptotic pathway of colonic epithelial cells, and to explore the role of SR-A1 mediated macrophages in impaired intestinal barrier of inflammatory bowel diseases (IBDs). Methods: Mouse macrophage RAW264.7 was pre-treated with SR-A1 antibody in the presence of lipopolysaccharide (LPS). Transwell system was employed for co-culture of RAW264.7 and Caco-2 in the presence of LPS and IFN-γ, with or without SR-A1 antibody pre-treatment. The percentage of F4/80 + CD11c + macrophages, apoptosis rate of Caco-2 cells, and expression of apoptosis and tight junction proteins in Caco-2 cells was determined. Results: Pre-treatment with SR-A1 antibody up-regulated IL-10 expression in RAW264.7, whereas down- regulated the expression of TNF and iNOS. Immunofluorescence staining indicated the upregulation of NF-κB p-p56 after LPS stimulation was significantly inhibited in the presence of SR-A1 antibody. The increase in p-JNK expression was inhibited by SR-A1 antibody. Transwell assay showed the percentage of F4/80+CD11c+ macrophages and apoptotic Caco-2 cells increased after treatment with LPS and IFN-γ, which could be reversed in the presence of SR-A1 antibody. The induction of cleaved caspase-3 and claudin-1 in Caco-2 cells was also suppressed when SR-A1 antibody pre-treatment. Conclusions: Pre-treatment with SR-A1 antibody can inhibit inflammatory response in LPS-induced macrophages in a NF-κB dependent manner. Pre-treatment with SR-A1 antibody also inhibits M1 phenotype expression of macrophages, and attenuates the pro-apoptotic effect on colonic epithelial cells and disruption of intestinal barrier integrity induced by macrophages. UR - https://atm.amegroups.org/article/view/34523