BACKGROUND/ PURPOSE: Triggering receptor expressed on myeloid cells-1 (TREM-1) is a regulator of immunity and an amplifier of inflammatory signaling. The aim was to clarify the role of TREM-1 in the pathophysiology of experimental severe acute pancreatitis (SAP). METHODS: SAP was induced by retrograde injection of 3 and 20% sodium deoxycholate (DCA) into the biliopancreatic ducts in rats (DCA pancreatitis). Soluble TREM-1 levels in serum, ascitic fluid, pancreas, liver and kidney were determined with an established available enzyme-linked immunosorbent assay (ELISA) kit. To clarify the source of soluble TREM-1 in serum and ascitic fluid, peritoneal macrophage depletion was done. Moreover, the effect of blockade of TREM-1 pathway was examined using LP17 (a synthetic TREM-1 inhibitor). RESULTS: Soluble TREM-1 levels in serum and ascitic fluid were higher in SAP. Membrane-bound TREM-1 protein was increased in pancreas, liver and kidney in SAP. Peritoneal macrophage depletion resulted in the reduction of soluble TREM-1 levels in serum and ascitic fluid. Pretreatment with LP17 improved the hepatic and renal dysfunction (serum aspartate aminotransferase and blood urea nitrogen levels) in SAP. CONCLUSIONS: TREM-1 may act as an important mediator for inflammation and organ injury in SAP. TREM-1 may be a potential therapeutic target for the development of SAP and associated organ dysfunction.
BACKGROUND/ PURPOSE:Triggering receptor expressed on myeloid cells-1 (TREM-1) is a regulator of immunity and an amplifier of inflammatory signaling. The aim was to clarify the role of TREM-1 in the pathophysiology of experimental severe acute pancreatitis (SAP). METHODS:SAP was induced by retrograde injection of 3 and 20% sodium deoxycholate (DCA) into the biliopancreatic ducts in rats (DCApancreatitis). Soluble TREM-1 levels in serum, ascitic fluid, pancreas, liver and kidney were determined with an established available enzyme-linked immunosorbent assay (ELISA) kit. To clarify the source of soluble TREM-1 in serum and ascitic fluid, peritoneal macrophage depletion was done. Moreover, the effect of blockade of TREM-1 pathway was examined using LP17 (a synthetic TREM-1 inhibitor). RESULTS: Soluble TREM-1 levels in serum and ascitic fluid were higher in SAP. Membrane-bound TREM-1 protein was increased in pancreas, liver and kidney in SAP. Peritoneal macrophage depletion resulted in the reduction of soluble TREM-1 levels in serum and ascitic fluid. Pretreatment with LP17 improved the hepatic and renal dysfunction (serum aspartate aminotransferase and blood ureanitrogen levels) in SAP. CONCLUSIONS:TREM-1 may act as an important mediator for inflammation and organ injury in SAP. TREM-1 may be a potential therapeutic target for the development of SAP and associated organ dysfunction.
Authors: Zheng Lu; Yan Liu; Yuan-hang Dong; Xian-bao Zhan; Yi-qi Du; Jun Gao; Yan-fang Gong; Zhao-shen Li Journal: Intensive Care Med Date: 2011-10-27 Impact factor: 17.440