Immunological aspects of COPD: A new approach to the issue [Aspetti immunologici della BPCO: Un nuovo approccio al problema]

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality throughout the world 1. It affects about 10% of the general population, but its prevalence increases considerably among heavy smokers. COPD is the fourth leading cause of death in most industrialized countries, after cardiovascular conditions, cancer and cerebrovascular disease 1. Tobacco smoking is by far the most important risk factor for the development of COPD; but exposure to particle or gases at work or burning biomass fuels for cooking and heating in developing countries have also been implicated. The association between COPD and smoking is not an absolute one. Indeed, COPD can develop in subjects without significant exposure to cigarette smoke or other known irritants. Furthermore, only a proportion of heavy smokers (ranging from 15 to 30%) would develop overt airflow obstruction and symptoms, suggesting that other traits may contribute to disease development. The defining feature of COPD is a limitation to expiratory airflow, typically progressive and not fully reversible, due to remodelling of peripheral airways and destruction of the lung parenchyma. These structural changes are associated with an abnormal inflammatory response in both the small airways and alveolar walls. It is well known that all smokers develop an acute inflammatory reaction, that is the expected response to the burden of irritants present in cigarette smoke. However, in COPD, this process is dramatically amplified; it escapes the normal mechanisms of control and arises independently of cigarette smoke. Indeed, for a given level of smoke exposure, the infiltration of inflammatory cells increases progressively with disease severity and persists for years after cessation of the smoking habit. Recent findings suggest that activation of the immune response could be a key component of COPD pathogenesis, pointing out the involvement of autoimmune mechanisms triggered by cigarette smoking 2.