title: Acute exacerbations of COPD: is inflammation central to prevention and treatment strategies?
abstract: Acute exacerbations (AE) represent one of the hallmarks of Chronic Obstructive Pulmonary Disease (COPD). They are characterised by increased from baseline dyspnoea, cough and sputum production and/or purulence, variably associated with fever and systemic symptoms. As in stable COPD, airway inflammation is an important part of the disease underlying the clinical manifestations. Studies on airway inflammation in AE by means of invasive methodologies (e.g. fiberoptic bronchoscopy with bronchial biopsy and/or bronchoalveolar lavage) are difficult due to clinical, practical and ethical issues. New and less- (sputum) or non-invasive methodologies (exhaled markers) are becoming increasingly applied also to the study of AE in COPD. The overall data on airway inflammation during AE seems to indicate an "acute on chronic" picture of inflammation, with increased proportions of inflammatory cells in tissue and lavage/sputum samples and with the change in the proportions of some of the cell types, such as a substantial increase in the numbers of eosinophils. Cytokines and inflammatory mediators involved in AE seem to be those related to PMN chemotaxis (IL-8 and LT) and those related to eosinophilic inflammation. A more precise categorisation of the event causing AE (e.g. viral vs. bacterial), and of the baseline patients' characteristics (e.g. severe vs. mild-moderate stage) associated with a wider application of well-standardised non-invasive methodologies could bring us in the future better clues on the pattern of airway inflammation during AE.
authors.affiliation: Divisione di Pneumologia Riabilitativa, Fondazione Salvatore Maugeri, I.R.C.C.S., Via Pinidolo 23, 25064 Gussago, Brescia, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Delmastro
authors.forename: B
authors.initials: B
authors.lastname: Balbi
mesh_terms: D001980:Bronchi / Q000503:physiopathology; D001999:Bronchoscopy; D018925:Chemokines / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D004804:Eosinophils / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy; D013183:Sputum / Q000737:chemistry
chemical_list: D018925:Chemokines; D016207:Cytokines