title: Reactive oxygen species (ROS) and wound healing: the functional role of ROS and emerging ROS-modulating technologies for augmentation of the healing process.
abstract: Reactive oxygen species (ROS) play a pivotal role in the orchestration of the normal wound-healing response. They act as secondary messengers to many immunocytes and non-lymphoid cells, which are involved in the repair process, and appear to be important in coordinating the recruitment of lymphoid cells to the wound site and effective tissue repair. ROS also possess the ability to regulate the formation of blood vessels (angiogenesis) at the wound site and the optimal perfusion of blood into the wound-healing area. ROS act in the host's defence through phagocytes that induce an ROS burst onto the pathogens present in wounds, leading to their destruction, and during this period, excess ROS leakage into the surrounding environment has further bacteriostatic effects. In light of these important roles of ROS in wound healing and the continued quest for therapeutic strategies to treat wounds in general and chronic wounds, such as diabetic foot ulcers, venous and arterial leg ulcers and pressure ulcers in particular, the manipulation of ROS represents a promising avenue for improving wound-healing responses when they are stalled. This article presents a review of the evidence supporting the critical role of ROS in wound healing and infection control at the wound site, and some of the new emerging concepts associated with ROS modulation and its potential in improving wound healing are discussed.
authors.affiliation: Institute of Skin Integrity and Infection Prevention, University of Huddersfield, Huddersfield, UK.|Department of Biological Sciences, School of Applied Sciences, University of Huddersfield, Huddersfield, UK.
authors.forename: Christopher
authors.initials: C
authors.lastname: Dunnill
authors.affiliation: Institute of Technology, Sligo, Ireland.
authors.forename: Thomas
authors.initials: T
authors.lastname: Patton
authors.affiliation: Institute of Technology, Sligo, Ireland.
authors.forename: James
authors.initials: J
authors.lastname: Brennan
authors.affiliation: Institute of Technology, Sligo, Ireland.
authors.forename: John
authors.initials: J
authors.lastname: Barrett
authors.affiliation: Department of Microbiology, Hampshire Hospitals NHS Foundation Trust, Winchester, UK.|Rare and Imported Pathogens Laboratory (RIPL), Public Health England, Porton Down, UK.
authors.forename: Matthew
authors.initials: M
authors.lastname: Dryden
authors.affiliation: Centre for Infection Prevention and Management, Division of Medicine, Imperial College, London, UK.|Manchester Pharmacy School, Faculty of Medical and Human Sciences, University of Manchester, Manchester, UK.
authors.forename: Jonathan
authors.initials: J
authors.lastname: Cooke
authors.affiliation: Institute of Skin Integrity and Infection Prevention, University of Huddersfield, Huddersfield, UK.
authors.forename: David
authors.initials: D
authors.lastname: Leaper
authors.affiliation: Institute of Skin Integrity and Infection Prevention, University of Huddersfield, Huddersfield, UK.|Department of Biological Sciences, School of Applied Sciences, University of Huddersfield, Huddersfield, UK.
authors.forename: Nikolaos T
authors.initials: NT
authors.lastname: Georgopoulos
mesh_terms: D049109:Cell Proliferation / Q000187:drug effects*; D006801:Humans; D017382:Reactive Oxygen Species / Q000627:therapeutic use*; D014945:Wound Healing / Q000502:physiology*; D014946:Wound Infection / Q000628:therapy*; D014947:Wounds and Injuries / Q000628:therapy*
chemical_list: D017382:Reactive Oxygen Species
keywords: Host defence; Reactive oxygen species; Wound healing; Wound infection