title: The Triggering Receptor Expressed on Myeloid cells-1: A new player during acute myocardial infarction.
abstract: Following myocardial ischemia, an intense activation of the immune system occurs that leads to inflammatory cytokines and chemokines production and to the recruitment of neutrophils and mononuclear cells in the infarcted area. Although pro-inflammatory signals initiate the cellular events necessary for scar formation, excessive and prolonged inflammation promotes deleterious cardiac remodeling and dysfunction. The triggering receptor expressed on myeloid cells-1 (TREM-1) is a highly conserved immune-receptor expressed by neutrophils and monocytes that acts as an amplifier of the innate immune response. Blockade of TREM-1 activation protects from hyper-responsiveness and death during severe infections. Here we review the role of TREM-1 in orchestrating the inflammatory response that follows MI. TREM-1 deletion (Trem-1-/-) or modulation by the use of a short inhibitory peptide (LR12) dampens myocardial inflammation, limits leukocyte recruitment, and improves heart function and survival in mice or pigs. Moreover, the soluble form of TREM-1 (sTREM-1) is found in the plasma of patients suffering from an acute MI and its concentration is an independent predictor of death. This suggests that TREM-1 may constitute a new therapeutic target during acute MI.
authors: Service de Réanimation Médicale, Hôpital Central, CHU Nancy, Université de Lorraine, Nancy, France; Inserm UMR_S1116, Faculté de Médecine de Nancy, Université de Lorraine, Vandoeuvre-les-Nancy, France.
authors: Lemarié
authors: L
authors: Jérémie
authors: INOTREM SA, Nancy, France.
authors: Boufenzer
authors: B
authors: Amir
authors: INOTREM SA, Nancy, France.
authors: Derive
authors: D
authors: Marc
authors: Service de Réanimation Médicale, Hôpital Central, CHU Nancy, Université de Lorraine, Nancy, France; Inserm UMR_S1116, Faculté de Médecine de Nancy, Université de Lorraine, Vandoeuvre-les-Nancy, France. Electronic address: s.gibot@chu-nancy.fr.
authors: Gibot
authors: G
authors: Sébastien
mesh_terms: D000208:Acute Disease; D000818:Animals; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D007850:Lauric Acids / Q000378:metabolism; D007962:Leukocytes / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism; D022423:Myeloid Cells / Q000378:metabolism*; D009203:Myocardial Infarction / Q000378:metabolism*; D009842:Oligopeptides; D011971:Receptors, Immunologic / Q000378:metabolism; D012235:Rhodamines / Q000378:metabolism; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
chemical_list: D007850:Lauric Acids; D008562:Membrane Glycoproteins; D009842:Oligopeptides; D011971:Receptors, Immunologic; D012235:Rhodamines; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; C420324:nangibotide
keywords: Inflammation; Myocardial infarction; TREM-1