Figure 2. The pro-resolving/pro-repair neutrophil.

Neutrophils use different strategies to initiate tissue repair, which often occur simultaneously or sequentially. From left to right: Neutrophils undergo apoptosis and expose “eat-me” signals such as phosphatidylserine on the cell surface, leading to phagocytosis by resident macrophages and inducing a pro-repair feed-forward loop. Neutrophils phagocytose debris, thereby clearing the injury site of proinflammatory stimuli, removing dead tissue, and making channels for angiogenesis. Neutrophils release numerous mediators that promote angiogenesis and tissue repair and modulate the inflammatory milieu. Neutrophils release microvesicles containing AnxA1. These microvesicles dampen further neutrophil recruitment and induce macrophage phenotype switching toward a repair phenotype. Neutrophils express receptors such as CCR5 that can function as cytokine scavengers to reduce the availability of proinflammatory cytokines for other neutrophils. Neutrophils release NETs, which can trap proinflammatory chemokines.