Autoimmunity and Mitochondrial Dysfunction in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. While other diseases associated with smoking have entered a plateau with respect to mortality, mortality associated with COPD has been increasing. Several facts seem to explain this phenomenon such as the increase in smoking habits in developing countries, the increase in life expectancy in high-income countries, and the growing increase in COPD not associated with smoking. A very striking finding of the entity is that the deterioration in lung function and therefore in mortality, is not stopped by the fact of suspending exposure to the environmental noxa. This could also contribute to this increase in mortality. The explanations considered are two: frequent respiratory infections in these patients, which are the leading cause of exacerbations, generate endogenous oxidative stress due to mitochondrial respiration, which perpetuates the inflammatory process, although exogenous exposure is suspended. The other explanation is autoimmunity playing a pathogenic role in the development and evolution of COPD. This chapter, therefore, aims to review the evidence of the immunological phenomenon in COPD giving special emphasis to two aspects: autoimmunity generating COPD and the possible therapeutic avenues that can be derived from this perspective. This last aspect seems crucial, especially since the current treatment does not prevent the deterioration of lung function or reduce mortality. Mitochondrial dysfunction in COPD and its therapeutic implications are also discussed. At the end, some suggestions are made about future research.