Roles of chemokines in pancreatitis: A review

Figure 5 Molecular mechanisms involved in pancreatitis. The figure illustrates several chemokines molecular mechanisms for the pancreatitis. These include macrophage-mediated production of inflammatory cytokines to impair pancreatic cells, causing trypsin spillage that leads to multiple organ dysfunction, and chemokines to attract immune cells, such as T-cell chemokines CCL3, CCL4, CCL5, CCL17, and CCL22, and neutrophil chemokines CXCL2 and CXCL8. Simultaneously, activated T cells secrete CCL1 to attract neutrophils and fibroblasts. Proinflammatory factors secreted by injured cells, such as: CXCL1, CXCL2, CXCL5, oxygen free radicals, and trypsin, can also activate neutrophils. Activated neutrophils can directly secrete myeloperoxidase, reactive oxygen species, nicotinamide adenine dinucleotide phosphate oxidase, and granular enzymes to impair many organs. Macrophages also secrete CXCL9 to prevent fibrosis of the pancreas, CX3CL1 to promote pancreatic hyperplasia, and CXCL10 and CX3CL1 to inhibits direct damage of macrophages. IL: Interleukin; MPO: Myeloperoxidase; TLR: Toll-like receptor.