![]() ![]() Neutrophils are implicated not only in disease initiation but also in exacerbations. Following smoke exposure, patients have an influx of macrophages and neutrophils into the lung. ![]() Inflammation in Smoke ExposureĪn increase in inflammatory cells has been documented in the lungs of patients with emphysema. Under smoke exposure conditions, epithelial cells and recruited inflammatory cells produce proteinases and oxidants that cause lung damage through alveolar septal cell apoptosis and destruction of the extracellular matrix (ECM). It has been long accepted that cigarette smoke leads to airway inflammation, but cigarette smoke also activates epithelial cells to release pro-inflammatory mediators, which amplify inflammation. In patients with chronic obstructive pulmonary disease (COPD), pro-inflammatory and pro-destructive pathways are activated, at times independent of smoke exposure, and other anti-inflammatory, anti-oxidant, or repair pathways are down-regulated, all resulting in lung destruction. Lung injury in emphysema is a result of inflammatory and destructive processes in response to cigarette smoke exposure. Overview of Lung Injury in COPD: Types and Key Questions This session provided an overview of key aspects of smoke-induced lung injury in order to better understand potential targets for new therapies. The inhalation of cigarette smoke causes a variety of pro-inflammatory and oxidative stress cascades to be activated within the lung, with resultant protease production and alveolar cell apoptosis, all leading to lung destruction. There are a multitude of factors that influence disease susceptibility, initiation of injury and progression of disease. Lung injury in COPD is the result of many different pathogenic processes within the lung. Pathophysiology of emphysema and implications. Running Head: Pathophysiology of EmphysemaĪbbreviations: chronic obstructive pulmonary disease COPD extracellular matrix ECM mammalian target of rapamycin mTOR vascular endothelial growth factor, VEGFĬitation: Goldklang M, Stockley R. ![]()
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