Emerging roles of neutrophil-borne S100A8/A9 in cardiovascular inflammation

Gopalkrishna Sreejit, Ahmed Abdel Latif, Andrew J. Murphy, Prabhakara R. Nagareddy

Research output: Contribution to journalReview articlepeer-review

33 Scopus citations


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.

Original languageEnglish
Article number105212
JournalPharmacological Research
StatePublished - Nov 2020

Bibliographical note

Publisher Copyright:
© 2020 Elsevier Ltd


  • Cardiac Inflammation
  • DAMPs
  • Myocardial Infarction
  • Neutrophils
  • S100A8/A9

ASJC Scopus subject areas

  • Pharmacology


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