| Popis: |
Andrew J Ghio,1 Elizabeth N Pavlisko,2 Victor L Roggli,2 Nevins W Todd,3 Rahul G Sangani4 1Human Studies Facility, US Environmental Protection Agency, Chapel Hill, NC, 27514, USA; 2Department of Pathology, Duke University, Durham, NC, USA; 3Department of Medicine, University of Maryland, Baltimore, MD, 21201, USA; 4Department of Medicine, West Virginia University, Morgantown, WV, USACorrespondence: Andrew J GhioHuman Studies Facility, US Environmental Protection Agency, 104 Mason Farm Road, Chapel Hill, NC, USAEmail ghio.andy@epa.govAbstract: It is proposed that the mechanistic basis for non-neoplastic lung injury with cigarette smoking is a disruption of iron homeostasis in cells after exposure to cigarette smoke particle (CSP). Following the complexation and sequestration of intracellular iron by CSP, the host response (eg, inflammation, mucus production, and fibrosis) attempts to reverse a functional metal deficiency. Clinical manifestations of this response can present as respiratory bronchiolitis, desquamative interstitial pneumonitis, pulmonary Langerhans’ cell histiocytosis, asthma, pulmonary hypertension, chronic bronchitis, and pulmonary fibrosis. If the response is unsuccessful, the functional deficiency of iron progresses to irreversible cell death evident in emphysema and bronchiectasis. The subsequent clinical and pathological presentation is a continuum of lung injuries, which overlap and coexist with one another. Designating these non-neoplastic lung injuries after smoking as distinct disease processes fails to recognize shared relationships to each other and ultimately to CSP, as well as the common mechanistic pathway (ie, disruption of iron homeostasis).Keywords: iron, ferritins, pulmonary disease, chronic obstructive, pulmonary emphysema, chronic bronchitis, hypertension, pulmonary, pulmonary fibrosis |
