B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction
Yasmine Zouggari,Hafid Ait-Oufella,Hafid Ait-Oufella,Hafid Ait-Oufella,Philippe Bonnin,Tabassome Simon,Andrew P. Sage,Coralie L. Guerin,Coralie L. Guerin,José Vilar,José Vilar,Giuseppina Caligiuri,Dimitrios Tsiantoulas,Dimitrios Tsiantoulas,Ludivine Laurans,Ludivine Laurans,Edouard Dumeau,Edouard Dumeau,Salma Kotti,Patrick Bruneval,Patrick Bruneval,Israel F. Charo,Christoph J. Binder,Christoph J. Binder,Nicolas Danchin,Alain Tedgui,Alain Tedgui,Thomas F. Tedder,Jean-Sébastien Silvestre,Jean-Sébastien Silvestre,Ziad Mallat,Ziad Mallat +31 more
TLDR
It is shown that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6Chi monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration ofMyocardial function.Abstract:
Acute myocardial infarction is a severe ischemic disease responsible for heart failure and sudden death. Here, we show that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6C(hi) monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration of myocardial function. Genetic (Baff receptor deficiency) or antibody-mediated (CD20- or Baff-specific antibody) depletion of mature B lymphocytes impeded Ccl7 production and monocyte mobilization, limited myocardial injury and improved heart function. These effects were recapitulated in mice with B cell-selective Ccl7 deficiency. We also show that high circulating concentrations of CCL7 and BAFF in patients with acute myocardial infarction predict increased risk of death or recurrent myocardial infarction. This work identifies a crucial interaction between mature B lymphocytes and monocytes after acute myocardial ischemia and identifies new therapeutic targets for acute myocardial infarction.read more
Citations
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Journal ArticleDOI
The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis
TL;DR: The renin-angiotensin-aldosterone system and members of the transforming growth factor-β family play an important role in activation of infarct myofibroblasts, and therapeutic modulation of the inflammatory and reparative response may hold promise for the prevention of postinfarction heart failure.
Journal ArticleDOI
The inflammatory response in myocardial injury, repair, and remodelling.
TL;DR: Biomarker-based approaches are needed to identify patients with distinct pathophysiologic responses and to rationally implement inflammation-modulating strategies in patients with myocardial infarction.
Journal ArticleDOI
Myocarditis and inflammatory cardiomyopathy: current evidence and future directions.
Carsten Tschöpe,Enrico Ammirati,Biykem Bozkurt,Biykem Bozkurt,Alida L.P. Caforio,Leslie T. Cooper,Stephan B. Felix,Joshua M. Hare,Bettina Heidecker,Stephane Heymans,Stephane Heymans,Norbert Hubner,Sebastian Kelle,Karin Klingel,Henrike Maatz,Abdul Shokor Parwani,Frank Spillmann,Randall C. Starling,Hiroyuki Tsutsui,Petar M. Seferovic,Sophie Van Linthout +20 more
TL;DR: Improved standardization of available invasive and noninvasive diagnostic tools and a consensus on their specific use are needed to allow specific diagnosis and stratification of patient cohorts for the implementation of aetiology-based therapies.
Journal ArticleDOI
Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities.
Sang Bing Ong,Sauri Hernández-Reséndiz,Gustavo E. Crespo-Avilan,Regina T. Mukhametshina,Xiu Yi Kwek,Hector A. Cabrera-Fuentes,Derek J. Hausenloy +6 more
TL;DR: An overview of the multiple players (and their dynamic roles) involved in the complex inflammatory response to AMI and subsequent LV remodeling is provided, and future opportunities for targeting inflammation as a therapeutic strategy for limiting MI size, preventing adverse left ventricular remodeling, and reducing heart failure in AMI patients are highlighted.
Journal ArticleDOI
Role of innate and adaptive immune mechanisms in cardiac injury and repair
TL;DR: The role of theimmune system in cardiovascular disease is summarized, focusing on the idea that the immune system evolved to promote tissue homeostasis following injury and/or infection, and that the inherent cost of this evolutionary development is unwanted inflammatory damage.
References
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Journal ArticleDOI
Myocardial Reperfusion Injury
TL;DR: This review focuses on the mechanisms of the injury, on attempts to protect the heart against it, and on promising new approaches to cardioprotection during percutaneous coronary intervention.
Journal ArticleDOI
The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions
Matthias Nahrendorf,Filip K. Swirski,Elena Aikawa,Lars Stangenberg,Thomas Wurdinger,Jose-Luiz Figueiredo,Peter Libby,Peter Libby,Ralph Weissleder,Mikael J. Pittet +9 more
TL;DR: This work identifies two distinct phases of monocyte participation after MI and proposes a model that reconciles the divergent properties of these cells in healing and identifies new therapeutic targets that can influence healing and ventricular remodeling after MI.
Journal ArticleDOI
Genetic Determinants of Response to Clopidogrel and Cardiovascular Events
Tabassome Simon,Céline Verstuyft,Murielle Mary-Krause,Lina Quteineh,Elodie Drouet,Nicolas Meneveau,P. Gabriel Steg,Jean Ferrières,Nicolas Danchin,Laurent Becquemont,Abstr Act +10 more
TL;DR: Among patients with an acute myocardial infarction who were receiving clopidogrel, those carrying CYP2C19 loss-of-function alleles had a higher rate of subsequent cardiovascular events than those who were not, particularly marked among the patients undergoing percutaneous coronary intervention.
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