Abstract
Markers of oxidative stress are increased in chronic obstructive pulmonary disease (COPD) and reactive oxygen species (ROS) are able to alter biological molecules, signaling pathways and antioxidant molecule function, many of which have been implicated in the pathogenesis of COPD. However, the involvement of ROS in the development and progression of COPD is not proven. Here, we discuss the sources of ROS, and the defences that have evolved to protect against their harmful effects. We address the role that ROS may have in the development and progression of COPD, as well as current therapeutic attempts at limiting the damage they cause. Evidence has indicated that the function of several key cells appears altered in COPD patients, and expression levels of important oxidant and antioxidant molecules may be abnormal. Therapeutic trials attempting to restore equilibrium to these molecules have not impacted upon all facets of disease and whilst the theory behind ROS influence in COPD appears sound, current models testing relevant pathways to tissue damage are limited. The heterogeneity seen in COPD patients presents a challenge to our understanding, and further research is essential to identify potential targets and stratified COPD patient populations where ROS therapies may be maximally efficacious.
Highlights
Chronic obstructive pulmonary disease (COPD) is a chronic respiratory lung condition with significant systemic manifestations and associated co-morbidities that deleteriously impacts on quality of life [1]
Neutrophils from COPD patients have been shown to release increased amounts of reactive oxygen species (ROS) spontaneously [59] and following stimulation [59,60,61]. These altered functions provide a possible mechanism for the damage seen in COPD; as neutrophils migrate through lung tissues they are known to release proteinases and ROS in sequence as they move through complex tissues
Epithelial cells within the lung are likely to have an impact upon COPD progression, whilst there is little evidence of abnormal ROS production from the cells directly, lung epithelial cells are capable of contributing to the pro-inflammatory environment that is key to ROS production
Summary
Chronic obstructive pulmonary disease (COPD) is a chronic respiratory lung condition with significant systemic manifestations and associated co-morbidities that deleteriously impacts on quality of life [1]. 15%–20% of smokers develop COPD and cessation of smoking does not halt progression of the disease, with continued evidence of inflammatory cell recruitment to the lungs (in particular neutrophil recruitment) and oxidative stress [6]. This indicates a self-perpetuating endogenous source of inflammation in susceptible individuals [7,8]. Oxidative stress occurs when exposure to free radicals is sufficient to overwhelm antioxidant defences Such free radicals, termed reactive oxygen species (ROS), are ubiquitous, arising during mitochondrial respiration, signaling and when contributing to the damage and destruction of pathogens. Evidence for pro- and anti-inflammatory imbalances that may lie at the heart of ROS involvement in COPD, and attempts to mitigate these via therapeutic treatments are discussed
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