Up-regulation of Gr1CD11b cell population in the spleen of NaClO-administered mice works to repair skin wounds

Neutrophils and macrophages engulf not only microorganisms but also damaged tissue and degrade these materials in the phagolysosome (1-5). In wound healing, early infiltration of neutrophils followed by macrophage infiltration are important defense mechanisms for repair of tissue damage. Infiltrating neutrophils clear the wounded area of foreign particles and bacteria and are then extruded with the eschar or phagocytosed by macrophages. Subsequent to neutrophil invasion, monocytes infiltrate the wound site and become activated macrophages that release growth factors such as platelet-derived growth factor and vascular endothelial growth factor, which initiate the formation of granulation tissue [6,7]. Recently, it has been shown that damage associated molecular patterns (DAMPs) from injured tissues cause innate cell activation [8-10]. Wounding induces death of tissue cells, which occurs upon the loss of plasma membrane integrity, thereby allowing the escape of intracellular material from the cells including heat shock proteins (HSPs), high-mobility group box protein 1 (HMGB1), ATP and uric acid. These intracellular materials, along with extracellular materials such as hyaluronan and heparin sulphate produced by proteolytic activity of dying cells, bind to pattern recognition receptors (PRRs) of resident macrophages and dendritic cells. Reactive oxygen species (ROS) are also produced upon wounding and have been shown to activate the inflammasome [8]. Activated cells produce inflammatory cytokines and chemokines, especially IL-8, which induces the migration of neutrophils to wounds. Migrated neutrophils are also activated by DAMPs and Up-regulation of Gr1CD11b cell population in the spleen of NaClO-administered mice works to repair skin wounds