Neutrophils are attracted to and generate denseswarms at sites of cell damage in diverse tissues,often extending the local disruption of organ architectureproduced by the initial insult. Whether the inflammatorydamage resulting from such neutrophilaccumulation is an inescapable consequence ofparenchymal cell death has not been explored. Usinga combination of dynamic intravital imaging andconfocal multiplex microscopy, we report here thattissue-resident macrophages rapidly sense thedeath of individual cells and extend membrane processesthat sequester the damage, a process thatprevents initiation of the feedforward chemoattractantsignaling cascade that results in neutrophilswarms. Through this ‘‘cloaking’’ mechanism, theresident macrophages prevent neutrophil-mediatedinflammatory damage,maintaining tissue homeostasisin the face of local cell injury that occurs on a regularbasis in many organs because of mechanical andother stresses