EGF-EGFR信号调节放射损伤中肠道巨噬细胞与Lgr5+干细胞的相互作用

o investigate the intestinal lamina propria macrophages interacting with Lgr5 + stem cells during the process of radiation intestinal injury. In this study, we used x-ray to irradiate mouse abdomen with 15Gy to establish the model of intestinal injury. Lgr5 + stem cells were obtained by Magnetic beads sorting experiment. The purity of Lgr5 + was determined by Western blot. The expression of cytokines and chemokines before and after irradiation with Lgr5 + cells was detected by Proteome Profiler technique. The expression of CD68 and epidermal growth factor receptor (EGFR) was detected by double immunofluorescence assay in colorectal tissues. The results showed that the percentage of intestinal macrophages migrating to the bottom of the crypt was the highest at 6 h after irradiation in mice. The expression of epidermal growth factor (EGF), IL-28A/B and Reg3g (regenerative islet-derived protein 3 gamma) in Lgr5 + stem cells were increased after irradiation, and there was a co-expression of CD68 and EGFR in the tissue. Lgr5 + stem cells produce more EGF after irradiation, promote the migration of intestinal macrophages and bind to EGFR expressed by macrophages, and initiate EGF-EGFR, the signal regulates the interaction of intestinal macrophages with Lgr5 + stem cells in radiation injury.