Temporal neutrophil polarization following myocardial infarction

Ma, Yonggang; Yabluchanskiy, Andriy; Iyer, Rugmani Padmanabhan; Cannon, Presley L.; Flynn, Elizabeth R.; Jung, Mira; Henry, Jeffrey B.; Cates, Courtney; DeLeon‐Pennell, Kristine Y.; Lindsey, Merry L.

doi:10.1093/cvr/cvw024

Cited by 284 publications

(316 citation statements)

References 40 publications

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“…Neutrophil infiltration peaks on day 1 post-AMI, and then gradually decreases (6). Necrotic cardiomyocytes and activated neutrophils release specific proteins that signal the presence of tissue injury, called danger-associated molecular patterns (DAMPs) or alarmins (7).…”

Section: Days 1-3: Neutrophilsmentioning

confidence: 99%

“…In-vitro treatment of neutrophils with cardiac cell lysate enriched in the HMGB1 and HSP60 alarmins predominantly polarized the cells towards a N1 phenotype. This effect was inhibited by a TLR4 blocking antibody, suggesting that TLR4 mediates alarmin-induced polarization of infiltrating neutrophils towards the pro-inflammatory subtype (6).…”

mentioning

confidence: 96%

“…Recent data by Ma et al revealed for the first time that two different neutrophil sub-populations are present in the infarcted myocardium during the first 7 days post-AMI: the N1 and the N2 neutrophil subsets (6). N1 neutrophils are characterized by high expression of genes encoding the pro-inflammatory proteins Ccl3, Il1β, Il12a and Tnfα, which are predominantly upregulated during the first 7 days after the AMI.…”

mentioning

confidence: 99%

“…N1 neutrophils are characterized by high expression of genes encoding the pro-inflammatory proteins Ccl3, Il1β, Il12a and Tnfα, which are predominantly upregulated during the first 7 days after the AMI. N1 neutrophils are the most abundantly present neutrophils, representing >80% of the total neutrophil population into the infarcted myocardium (6). In contrast, N2 neutrophils preferentially express the anti-inflammatory Arg1, Cd206, Il10 and Tgfβ genes, and their presence gradually increases during the first week post-AMI from around 2.5% on day 1 to 18% on day 7 (6 -).…”

mentioning

confidence: 99%

“…N1 neutrophils are the most abundantly present neutrophils, representing >80% of the total neutrophil population into the infarcted myocardium (6). In contrast, N2 neutrophils preferentially express the anti-inflammatory Arg1, Cd206, Il10 and Tgfβ genes, and their presence gradually increases during the first week post-AMI from around 2.5% on day 1 to 18% on day 7 (6 -). In-vitro treatment of neutrophils with cardiac cell lysate enriched in the HMGB1 and HSP60 alarmins predominantly polarized the cells towards a N1 phenotype.…”

mentioning

confidence: 99%

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Innate Immune Mechanisms in Myocardial Infarction - An Update

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Marinković

Cotoi

et al. 2018

Revista Romana De Medicina De Laborator

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Section: Days 1-3: Neutrophilsmentioning

confidence: 99%

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confidence: 96%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Innate Immune Mechanisms in Myocardial Infarction - An Update

Mareş

Marinković

Cotoi

et al. 2018

Revista Romana De Medicina De Laborator

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Photopolymerizable Hydrogel for Enhanced Intramyocardial Vascular Progenitor Cell Delivery and Post‐Myocardial Infarction Healing

Hong,

Luo,

Doulamis

et al. 2023

Adv Healthcare Materials

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Cell transplantation success for myocardial infarction (MI) treatment is often hindered by low engraftment due to washout effects during myocardial contraction. A clinically viable biomaterial that enhances cell retention could optimize intramyocardial cell delivery. In this study, we developed a therapeutic cell delivery method for MI treatment utilizing a photocrosslinkable gelatin methacryloyl (GelMA) hydrogel. Human vascular progenitor cells, capable of forming functional vasculatures upon transplantation, were combined with an in‐situ photopolymerization approach and injected into the infarcted zones of mouse hearts. Our strategy substantially improved acute cell retention and promoted long‐term post‐MI cardiac healing, including stabilized cardiac functions, preserved viable myocardium, and reduced cardiac fibrosis. Additionally, engrafted vascular cells polarized recruited bone marrow‐derived neutrophils toward a non‐inflammatory phenotype via TGFβ signaling, fostering a pro‐regenerative microenvironment. Neutrophil depletion negated the therapeutic benefits generated by cell delivery in ischemic hearts, highlighting the essential role of non‐inflammatory, pro‐regenerative neutrophils in cardiac remodeling. In conclusion, our GelMA hydrogel‐based intramyocardial vascular cell delivery approach holds promise for enhancing the treatment of acute myocardial infarction.This article is protected by copyright. All rights reserved

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Gut microbiota‐related modulation of immune mechanisms in post‐infarction remodelling and heart failure

Roessler,

Zimmermann,

Heidecker

et al. 2024

ESC Heart Failure

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The immune system has long been recognized as a key driver in the progression of heart failure (HF). However, clinical trials targeting immune effectors have consistently failed to improve patient outcome across different HF aetiologies. The activation of the immune system in HF is complex, involving a broad network of pro‐inflammatory and immune‐modulating components, which complicates the identification of specific immune pathways suitable for therapeutic targeting. Increasing attention has been devoted to identifying gut microbial pathways that affect cardiac remodelling and metabolism and, thereby impacting the development of HF. In particular, gut microbiota‐derived metabolites, absorbed by the host and transported to the peripheral circulation, can act as signalling molecules, influencing metabolism and immune homeostasis. Recent reports suggest that the gut microbiota plays a crucial role in modulating immune processes involved in HF. Here, we summarize recent advances in understanding the contributory role of gut microbiota in (auto‐)immune pathways that critically determine the progression or alleviation of HF. We also thoroughly discuss potential gut microbiota‐based intervention strategies to treat or decelerate HF progression.

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Temporal neutrophil polarization following myocardial infarction

Abstract: This study is the first to identify the existence of N1 and N2 neutrophils in the infarct region and reveals that N1 polarization could be mediated by DAMPs.

Cited by 284 publications

References 40 publications

Innate Immune Mechanisms in Myocardial Infarction - An Update

Innate Immune Mechanisms in Myocardial Infarction - An Update

Photopolymerizable Hydrogel for Enhanced Intramyocardial Vascular Progenitor Cell Delivery and Post‐Myocardial Infarction Healing

Gut microbiota‐related modulation of immune mechanisms in post‐infarction remodelling and heart failure

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