title: Redox regulation of neutrophil apoptosis and the systemic inflammatory response syndrome.
abstract: SIRS (systemic inflammatory response syndrome) may result from a wide variety of non-infective insults. Surgery is a recognized cause of SIRS, the onset of which can have adverse prognostic significance. Neutrophil activation is a key histopathological feature of SIRS, and neutrophil clearance through programmed cell death or apoptosis is an essential step in its resolution. Increasingly, it is recognized that ROS (reactive oxygen species), such as those generated by activated neutrophils during cardiac surgery, may have a regulatory role, influencing neutrophil lifespan and thus inflammation. In this review, we discuss the continuing importance of SIRS as a herald of inflammation and the role of neutrophil longevity in the resolution of inflammation, and we consider recent evidence for the regulation of neutrophil apoptosis by ROS.
authors.affiliation: Department of Critical Care Medicine, Imperial College, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK.
authors.forename: Daniel D
authors.initials: DD
authors.lastname: Melley
authors.forename: Timothy W
authors.initials: TW
authors.lastname: Evans
authors.forename: Gregory J
authors.initials: GJ
authors.lastname: Quinlan
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D006801:Humans; D018375:Neutrophil Activation; D009504:Neutrophils / Q000473:pathology / Q000502:physiology*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000503:physiopathology*
chemical_list: D017382:Reactive Oxygen Species