@article{JTD2184,
author = {Nikolaos Angelis and Konstantinos Porpodis and Paul Zarogoulidis and Dionysios Spyratos and Ioannis Kioumis and Antonis Papaiwannou and Georgia Pitsiou and Kosmas Tsakiridis and Andreas Mpakas and Stamatis Arikas and Theodora Tsiouda and Nikolaos Katsikogiannis and Ioanna Kougioumtzi and Nikolaos Machairiotis and Michael Argyriou and George Kessisis and Konstantinos Zarogoulidis},
title = {Airway inflammation in chronic obstructive pulmonary disease},
journal = {Journal of Thoracic Disease},
volume = {6},
number = {Suppl 1},
year = {2014},
keywords = {},
abstract = {Chronic obstructive pulmonary disease (COPD) is an inflammatory airway disease whose incidence and mortality increases every year. It is associated with an abnormal inflammatory response of the lung to toxic particles or gases (usually cigarette smoke). A central role in the pathophysiology has been shown to play a chronic inflammation of the airways that is expressed primarily by hypersecretion of mucus, stenosis of the smaller airways and the establishment of pulmonary emphysema. There is an increasing trend for assessing the inflammatory pattern of inflammatory airway diseases through mediators measured by noninvasive techniques. Markers in biological fluids and exhaled air have been the subject of intense evaluation over the past few years, with some of them reaching their introduction into clinical practice, while others remain as research tools. Of particular interest for the scientific community is the discovery of clinically exploitable biomarkers associated with specific phenotypes of the disease. Studying the effects of therapeutic interventions in these biomarkers may lead to targeted therapy based on phenotype and this is perhaps the future of therapeutics in COPD.},
issn = {2077-6624}, url = {https://jtd.amegroups.org/article/view/2184}
}