Neutrophils in Post-myocardial Infarction Inflammation: Damage vs. Resolution?

Abstract

Inflammation not only plays a crucial role in acute ischemic cardiac injury, but also contributes to post-infarction repair and remodeling. Traditionally, neutrophils have been merely considered as detrimental in the setting of an acute myocardial infarction. However, recently published studies demonstrated that neutrophils might also play an important role in cardiac repair by regulating reparative processes. An emerging concept is that different neutrophil subsets exist, which might exhibit separate functional properties. In support of the existence of distinct neutrophil subsets in the ischemic heart, transcriptional changes in cardiac neutrophils have been reported within the first few days after myocardial infarction. In addition, there is an increasing awareness of sex-specific differences in many physiological and pathophysiological responses, including cardiovascular parameters and inflammation. Of particular interest in this context are recent experimental data dissecting sex-specific differences in neutrophil signaling after myocardial infarction. Unraveling the distinct and possibly stage-dependent properties of neutrophils in cardiac repair may provide new therapeutic strategies in order to improve the clinical outcome for myocardial infarction patients. This review will briefly discuss recent advances in our understanding of the neutrophil functional repertoire and emerging insights of sex-specific differences in post-myocardial infarction inflammatory responses.

The Intrapericardial Delivery of Extracellular Vesicles from Cardiosphere-Derived Cells Stimulates M2 Polarization during the Acute Phase of Porcine Myocardial Infarction

“…These cells have been usually considered as pro-inflammatory cells and according to clinical outcomes in myocardial disease, the increase of circulating neutrophils after EV-CDCs administration could be correlated with an aggravated outcome [38]. On the contrary, there are evidences for the pro-regenerative and antiinflammatory capacity of these cells in myocardial infarction [27,39]. Considering this duality, the increase of circulating neutrophils after EV-CDCs treatment deserves further investigation and a full characterization of these neutrophils.…”

Effects of progranulin on the pathological conditions in experimental myocardial infarction model

“…A recent study have shown that excessive accumulation of neutrophils exacerbated myocardial infarct size 24 h after permanent occlusion of LCA 33 . In addition, attenuating the recruitment of neutrophils decreased the infarct size in permanent occlusion of LCA and myocardial I/R injury 31,34 . It is implicated that inhibition of neutrophil activation attenuates tissue injury after MI.…”

“…Neutrophils infiltrate the infarct area in the first few hours following onset of myocardial ischemia. They produce reactive oxygen species and granule components including myeloperoxidase, thereby exacerbating tissue injury 31 . On the other hand, a recent study has reported that infiltration of neutrophils were required to resolve inflammation post-MI 32 .…”

Ischemia/Reperfusion Injury: Pathophysiology, Current Clinical Management, and Potential Preventive Approaches

“…Despite the inflammatory, tissue-damaging role that neutrophils have on the acute phase of MIRS, after ≈7 days, the inflammatory Ly6G + CD206neutrophil population is replaced by a Ly6G + CD206 + population that has been described to play an important role in the orchestration of the reparative phase, as reviewed in [70]. Also, apoptotic neutrophils induce an M2 phenotype in infiltrated macrophages upon their phagocytosis, which inhibits the macrophage proinflammatory tissue-damaging response and leads them to produce IL-10 and TGF-β [71,72].…”