Related Experiment Video
Updated: Dec 7, 2025
Expression, Purification, and Antimicrobial Activity of S100A12
Published on: May 13, 2017
Emerging roles of neutrophil-borne S100A8/A9 in cardiovascular inflammation
Gopalkrishna Sreejit1, Ahmed Abdel Latif2, Andrew J Murphy3
1Division of Cardiac Surgery, Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Insights
Neutrophils and their alarmins, S100A8/A9, play dual roles in heart attack recovery, causing damage but also aiding inflammation resolution. Targeting neutrophils offers potential for better heart failure therapies.
Area of Science:
- Cardiovascular Science
- Immunology
- Inflammation Research
Background:
- Elevated neutrophil counts correlate with increased risk of major adverse cardiac events (MACE), including myocardial infarction (MI) and heart failure.
- Neutrophils contribute to cardiac damage via immune cell attraction and inflammatory mediator release.
- Neutrophil-derived alarmins, S100A8/A9, are implicated in MI-induced inflammation and cardiac injury.
Purpose of the Study:
- To review the dual role of neutrophil-derived S100A8/A9 in promoting inflammation and resolution post-myocardial infarction (MI).
- To explore therapeutic strategies targeting neutrophils for ameliorating cardiac inflammation and damage.
- To understand how neutrophils balance pro-inflammatory and resolution-promoting functions in MI.
Main Methods:
- Review of independent studies and scientific literature.
- Analysis of mechanisms of neutrophil-derived S100A8/A9 in cardiac inflammation and resolution.
- Exploration of potential therapeutic targets within neutrophil pathways.
Main Results:
- Neutrophil-derived S100A8/A9 are causally linked to inflammation and cardiac injury following MI.
- Serum S100A8/A9 levels correlate with MACE in MI patients.
- Neutrophils and S100A8/A9 also exhibit crucial roles in inflammation resolution, presenting a therapeutic paradox.
Conclusions:
- Neutrophils exert both detrimental and beneficial effects in myocardial infarction, mediated partly by S100A8/A9.
- Targeting neutrophils requires a nuanced approach to preserve beneficial functions while mitigating harmful inflammation.
- Further understanding of neutrophil mechanisms is key to developing effective therapies for heart failure post-MI.
Abstract:
Elevated neutrophil count is associated with higher risk of major adverse cardiac events including myocardial infarction and early development of heart failure. Neutrophils contribute to cardiac damage through a number of mechanisms, including attraction of other immune cells and release of inflammatory mediators. Recently, a number of independent studies have reported a causal role for neutrophil-derived alarmins (i.e. S100A8/A9) in inducing inflammation and cardiac injury following myocardial infarction (MI). Furthermore, a positive correlation between serum S100A8/A9 levels and major adverse cardiac events (MACE) in MI patients was also observed implying that targeting neutrophils or their inflammatory cargo could be beneficial in reducing heart failure. However, contradictory to this idea, neutrophils and neutrophil-derived S100A8/A9 also seem to play a vital role in the resolution of inflammation. Thus, a better understanding of how neutrophils balance these seemingly contrasting functions would allow us to develop effective therapies that preserve the inflammation-resolving function while restricting the damage caused by inflammation. In this review, we specifically discuss the mechanisms behind neutrophil-derived S100A8/A9 in promoting inflammation and resolution in the context of MI. We also provide a perspective on how neutrophils could be potentially targeted to ameliorate cardiac inflammation and the ensuing damage.
More Related Videos
11:21Bioparticle Microarrays for Chemotactic and Molecular Analysis of Human Neutrophil Swarming in vitro
Published on: February 16, 2020
11:22Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions
Published on: August 23, 2013
Related Concept Videos
01:38Inflammation
01:19Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
01:30Inflammatory Response I: Vascular and Cellular