Premium
Role of triggering receptor expressed on myeloid cells‐1 in experimental severe acute pancreatitis
Author(s) -
Kamei Keiko,
Yasuda Takeo,
Ueda Takashi,
Qiang Fu,
Takeyama Yoshifumi,
Shiozaki Hitoshi
Publication year - 2010
Publication title -
journal of hepato‐biliary‐pancreatic sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 1868-6974
DOI - 10.1007/s00534-009-0191-6
Subject(s) - acute pancreatitis , pancreas , inflammation , pancreatitis , kidney , peritoneal fluid , receptor , medicine , immunology , pharmacology
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.