The Triggering Receptor Expressed on Myeloid cells-1: A new player during acute myocardial infarction

Autor: Lemarié Jérémie, Derive Marc, Boufenzer Amir, Gibot Sébastien
Přispěvatelé: Service de Réanimation Médicale [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Faculté de Médecine [Nancy], Université de Lorraine (UL), INOTREM SA, Université de Lorraine (UL)-Université de Lorraine (UL)
Jazyk: angličtina
Rok vydání: 2015
Předmět:
MESH: Inflammation
Chemokine
TREM-1
Myeloid
MESH: Membrane Glycoproteins
MESH: Lauric Acids
Inflammation
030204 cardiovascular system & hematology
MESH: Rhodamines
Peripheral blood mononuclear cell
Proinflammatory cytokine
MESH: Leukocytes
03 medical and health sciences
0302 clinical medicine
Immune system
[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system
medicine
Leukocytes
Animals
Humans
Myeloid Cells
MESH: Animals
Receptors
Immunologic
Receptor
MESH: Receptors
Immunologic
030304 developmental biology
Pharmacology
0303 health sciences
Innate immune system
Membrane Glycoproteins
MESH: Humans
biology
business.industry
Rhodamines
Lauric Acids
MESH: Triggering Receptor Expressed on Myeloid Cells-1
MESH: Myeloid Cells
Triggering Receptor Expressed on Myeloid Cells-1
Myocardial infarction
MESH: Myocardial Infarction
medicine.anatomical_structure
Immunology
Acute Disease
biology.protein
MESH: Acute Disease
medicine.symptom
business
Oligopeptides
Zdroj: Pharmacological Research
Pharmacological Research, Elsevier, 2015, 100, pp.261-265. ⟨10.1016/j.phrs.2015.07.027⟩
ISSN: 1043-6618
1096-1186
Popis: International audience; 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.
Databáze: OpenAIRE
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