Editorial
Copyright ©2010 Baishideng Publishing Group Co.
World J Gastroenterol. Aug 28, 2010; 16(32): 3995-4002
Published online Aug 28, 2010. doi: 10.3748/wjg.v16.i32.3995
Figure 1
Figure 1 Our current understanding of the role of monocytes and macrophages in the pathogenesis of acute pancreatitis. Local inflammation in the pancreas leads to secretion of pro-inflammatory cytokines and some unknown factors. These inflammatory mediators activate peritoneal macrophages (PMO), Kupffer cells, and alveolar macrophages (AMO), which if uncontrolled can cause multiple organ dysfunction syndrome (MODS). PMO display a classical M1 type activation in acute pancreatitis thus supporting the inflammatory process. TNF: Tumor necrosis factor; RNI: Reactive nitrogen intermediates; ROI: Reactive oxygen intermediates; PAAF: Pancreatitis associated ascitic fluid; PAP: Pancreatitis-associated protein; MCP: Monocyte chemotactic protein-1; PG: Prostaglandins; LK: Leukotrienes; SIRS: Systemic inflammatory response syndrome; PMN: Polymorphonuclear leukocytes; MIP: Macrophage inflammatory protein.