Divergent Effects on Phagocytosis by Macrophage-Derived Oxygen Radicals

Clearance of senescent cells from damaged tissue is a crucial step to successfully resolve an inflammatory response. Poor clearance has been attributed to defects in neutrophil apoptosis, a process that is regulated in part by reactive oxygen species (ROS) produced by activated neutrophils. Using ROS-deficient and wild-type macrophages treated with extracellular ROS scavengers we demonstrate that macrophage-derived ROS also influence phagocytosis and do so by direct and indirect mechanisms.