日本血吸虫
分子生物学
免疫印迹
重组DNA
流式细胞术
转染
受体
生物
表达式向量
细胞培养
单核细胞
化学
细胞生物学
免疫学
基因
血吸虫病
生物化学
遗传学
蠕虫
作者
Pei Shen,Tianyu Zhang,Guo Chen,Bei Zhang,Ailong Huang,Lian Duan,Dandan Zhu,Jinling Chen,Jianxin Wang,Yinong Duan
标识
DOI:10.1016/j.biopha.2022.112826
摘要
Triggering receptor expressed on myeloid cells 1 (TREM-1) is a transmembrane glycoprotein receptor and TREM-1 expression reached the peak at 6 weeks after infection with Schistosoma japonicum and inhibited subsequently. Since TREM-1 may be involved in the macrophage polarization process, the reason for the inhibition of TREM-1 expression in chronic schistosomiasis engaged us in them. In this study, flow cytometry was used to observe TREM-1 expression in peritoneal macrophages from mice infected with Schistosoma japonicum. Since P40 is one of the main components from schistosoma eggs, western blot and dual-luciferase reporter assays were performed to observe the effect of recombinant Schistosoma japonicum P40 protein (rSjP40) on TREM-1 expression in the mouse leukemic monocyte/macrophage cell line RAW264.7. These methods were also conducted to observe the effect of FOXO3a on the expression of TREM-1 in RAW264.7 cells, and a ChIP assay was performed to confirm the binding site of FOXO3a to the TREM-1 promoter. Our results showed that TREM-1 expression reached the peak in peritoneal macrophages from mice at 6 weeks after infection with Schistosoma japonicum. rSjP40 inhibited TREM-1 promoter activity at the position of - 1924 ~ - 1531 bp. rSjP40 down-regulated TREM-1 and FOXO3a protein expression in RAW264.7 cells. TREM-1 protein expression may be regulated by binding of FOXO3a to the promoter of TREM-1 in RAW264.7 cells. In conclusion, we found that rSjP40 inhibited TREM-1 expression in macrophages by inhibiting FOXO3a expression. This study will provide the basis for the study to explore the role of TREM-1 in Schistosoma japonicum infection.
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