Neutrophil–macrophage cross-talk in acute myocardial infarction

This editorial refers to ‘Neutrophils orchestrate post-myocardial infarction healing by polarizing macrophages towards a reparative phenotype’, by M. Horckmans et al . on doi:10.1093/eurheartj/ehw002 Neutrophils are the first immune cells arriving at the site of infection or injury. These early responders are effective in fighting pathogens via several mechanisms: they phagocytose antibody- or complement-coated pathogens and kill them by NADPH oxidase-dependent mechanisms or antibacterial proteins that are released from granules into the phagosome. The content of these granules, i.e. various inflammatory mediators including neutrophil-derived lipocalin (NGAL), is also released to fight extracellular pathogens. Neutrophil extracellular traps (NETs), composed of chromatin, histones, and proteases, are yet another mechanism to capture and kill microorganisms.1 In sterile injury after ischaemia, danger-associated molecules released by necrotic tissues trigger the same Toll-like receptor-induced activation of neutrophils. After myocardial infarction (MI), neutrophils are the first to enter the damaged tissue in large numbers, and peak at day 1 after onset of ischaemia.2 While neutrophils initially help to clear cellular debris, their inflammatory mediators result in tissue damage and further leucocyte recruitment.3 Neutrophils may support recruitment and activation of Ly-6Chi monocytes,4 which dominate ischaemic tissue on days 1–4 after injury. Ly-6Chi monocytes are initially …