Neutrophil membrane-camouflaged nanoparticles alleviate inflammation and promote angiogenesis in ischemic myocardial injury

Acute myocardial infarction (AMI) induces a sterile inflammatory response, leading to cardiomyocyte damage and adverse cardiac remodeling. Interleukin-5 (IL-5) plays an essential role in developing eosinophils (EOS), which are beneficial for the resolution of inflammation. Furthermore, the proangiogenic properties of IL-5 also contribute to tissue healing following injury. Therefore, targeted delivery of IL-5 is an innovative therapeutic approach for treating AMI. It has been shown that conventional IL-5 delivery can result in undesirable adverse effects and potential drug overdose. In this study, we successfully synthesized a biomimetic IL-5 nanoparticle by camouflaging the IL-5 nanoparticle in a neutrophilic membrane. The administration of neutrophil membrane–camouflaged nanoparticles (NM-NPIL-5) in the in vivo model showed that these nanoparticles promoted EOS accumulation and angiogenesis in the infarcted myocardium, thereby limiting adverse cardiac remodeling after AMI. Our results also demonstrated that the NM-NPIL-5 could serve as neutrophil “decoys” to adsorb and neutralize the elevated neutrophil-related cytokines in the injured heart by inheriting multiple receptors from their “parent” neutrophils. Finally, the targeted delivery of NM-NPIL-5 protected the cardiomyocytes from excessive inflammatory-induced apoptosis and maintained cardiac function. Our findings provided a promising cardiac detoxification agent for acute cardiac injury. A neutrophile membrane-camouflaged nanoparticles (NM-NPIL-5) were fabricated to minimize cardiac injury by promoting angiogenesis and inhibiting inflammatory responses. [Display omitted] •A promising cardiac detoxification agent has been designed, optimized, and characterized.•A neutrophil membrane coating can absorb and neutralize elevated neutrophil-associated cytokines.•Membrane coating can facilitate adhesion to inflammatory endothelial cells and transmigration through the barrier.•A significant proangiogenic effect was observed when interleukin (IL)-5 was delivered into damaged myocardium.•Interleukin (IL)-5 released into circulation blood could promote EOS and M2-like polarization of macrophages post-MI.