Fig 1: Apoptotic intestinal epithelial cells induced activation of MerTK-ERK1/2 pathway in macrophages and M2-biased polarization(A) immunofluorescence staining of cleaved-caspase 3 in human specimens.(B) change in the MerTK pathway by western blot and corresponding grayscale analysis (compared to the control group) in Raw 264.7 cells after coculture with CT-26 cells exposed to different durations of 254-nm UV.(C) Transcriptional change in the MerTK pathway in RAW264.7 cells by qPCR analysis.(D) Western blotting of pro-caspase3/cleaved-caspase 3 expression at different exposure times in the NCM460 cell line and corresponding grayscale analysis (compared to the control group).(E) Western blotting and grayscale analysis (compared to the control group) of the MerTK pathway in cocultured PBMC-derived macrophages; 0–I: 0 min-stimulation with apoptotic MCM460 + GM-CSF induced PBMCs, which were extracted from patients with inflamed CD; 30–I: 30 min-stimulation with apoptotic NCM460 + GM-CSF induced PBMCs, which were extracted from patients with inflamed CD; 0–F: 0 min-stimulation with apoptotic MCM460 + GM-CSF induced PBMCs, which were extracted from patients with fibrostenotic CD; 30–F: 30 min-stimulation with apoptotic MCM460 + GM-CSF induced PBMCs, which were extracted from patients with fibrostenotic CD; 0–N: 0 min-stimulation with apoptotic MCM460 + GM-CSF induced PBMCs, which were extracted from healthy donors; 30–F: 30 min-stimulation with apoptotic MCM460 + GM-CSF induced PBMCs, which were extracted from healthy donors.(F) Evaluation of mRNA expression in PBMC-derived macrophages, extracted from patients with CD after coculture with UV-treated NCM460 cells (30 min). All in vitro experiments were repeated at least three times to minimize technical and biological variability.