Neutrophils are highly pro-inflammatory cells with well-established roles in pathogen clearance through phagocytosis, the release of antimicrobial factors and production of neutrophil extracellular traps. All these neutrophil functions can cause tissue damage and therefore must be tightly regulated. Hsu et al. report in Cell that as neutrophils age they actively release CD55+ vesicles that inhibit complement activation and thus help to resolve inflammation.

In a mouse model of acute Staphylococcus aureus-induced neutrophilic pneumonia, exogenous administration of purified neutrophil-derived large vesicles 1 hour after infection markedly reduced the number of neutrophils and levels of proinflammatory cytokines in the bronchoalveolar lavage fluid (BALF), which was associated with reduced lung pathology. In a model of lethal S. aureus-induced pneumonia, mice treated with the neutrophil vesicles had increased survival. The anti-inflammatory effect was specific to the ageing neutrophil-associated large vesicles and could not be recapitulated by administration of exosomes, microvesicles or apoptotic bodies.