Effects of the TREM-1 pathway modulation during mesenteric ischemia-reperfusion in rats

• DOI: 10.1097/01.ccm.0b013e318161faf3
• Publication Date: 2009-03-05T07:05:46Z
• Authors: Sébastien Gibot; Frédéric Massin; Corentine Alauzet; Chantal Montemont; Alain Lozniewski; Pierre-Edouard Bo...; Bruno Levy
• Keywords: Mesenteric lymph nodes; Pathogenesis

Objectives: The triggering receptor expressed on myeloid cells (TREM)-1, a the surface of neutrophils and monocytes/macrophages, synergizes with Toll-like receptors in amplifying inflammatory response mediated by microbial components. Because pathogenesis ischemia-reperfusion-induced gastrointestinal tissue injury multiple organ failure implies leukocyte activation bacterial translocation, we hypothesized that TREM-1 pathway modulation would prove beneficial this setting. Design: Animal study. Setting: Research laboratory. Subjects: Adult male Wistar rats (250–300 g). Interventions: Rats were subjected to intestinal ischemia-reperfusion induced occlusion superior mesenteric artery during 60 mins reperfused for 180 mins. At time reperfusion, animals administered LP17 (a synthetic inhibitor), control peptide, or vehicle (normal saline). Plasma concentrations tumor necrosis factor-α, interleukin-6, soluble measured enzyme-linked immunosorbent assay. Hepatic transcriptional factor nuclear factor-κB was assessed electrophoretic mobility shift oxidant-antioxidant balance estimated measurement lipid peroxidation catalase activity. Ileal mucosal permeability fluorescein dextran-4 clearance translocation lymph nodes culture. Measurements Main Results: Ischemia-reperfusion associated cardiovascular collapse, lactic acidosis, systemic hepatic partly prevented administration. Liver depletion attenuated LP17. marked increase ileal an also modulation. delayed mortality. Conclusions: means peptide may be useful acute ischemia.