Pathogenesis of respiratory inflammation Patogenesi dell'infiammazione respiratoria

Airways 'inflammation' plays a key role in the pathogenesis of airways disease and remodeling in COPD as well as in a number of other disease states including bronchial asthma, respiratory tract infections, cystic fibrosis, bronchiolitis and bronchiectasis. Inflammatory cells such as macrophages, neutrophils, eosinophils, CD8+ T lymphocytes, and subsequent changes which include epithelial damage and mucus hypersecretion have been investigated in a number of studies. Notably in COPD, which is also characterized by parenchymal destruction, the heterogeneity of the disease has hindered data interpretation, while extrapolation of the results of relatively non-invasive studies to the actual pathology found in the distal lung is difficult. Thus, major studies have frequently elicited conflicting interpretation, and a detailed profile of disease phenotype-specific inflammation of COPD as well as the importance of spill-over of inflammatory mediators into the circulating blood has yet to emerge. Further investigations are needed to link the different clinical and functional phenotypes of COPD to their respective inflammatory profiles in the airways thus improving the understanding of the pathogenesis of the disease as a whole. The acute effects of cigarette smoking on inflammation and oxidative stress in acute smoke exposure can result in tissue damage, as suggested by increased reactive oxygen species and products of lipid peroxidation and degradation of extracellular matrix proteins. Acute cigarette smoke exposure, however, has also a suppressive effect on the number of eosinophils and several inflammatory cytokines, possibly due to the anti-inflammatory effect of carbon monoxide. Hopefully, in the near future data from studies on airway and parenchymal inflammation in COPD will prove useful to identify and assess the causes, severity, prognosis, and response to treatment.