CCL5 and acute pancreatitis: Animal models and organoid cultures have demonstrated that pro-inflammatory, M1 polarized macrophages can drive ADM during acute pancreatitis, which was mediated through the secretion by macrophages of cytokines, e.g., TNF-α (tumor necrosis factor-alpha) and chemokines, e.g., CCL5/RANTES (regulated upon activation, normal T cell expressed and presumably secreted) [15].