Autoimmunity and Mitochondrial Dysfunction in Chronic Obstructive Pulmonary Disease

Abstract

Chronic obstructive pulmonary disease (COPD) includes several clinical syndromes, most notably emphysema and chronic bronchitis, respiratory bronchiolitis, asthma and COPD overlap syndrome (ACOS), COPD and obstructive sleep apnea (OSA) overlap syndrome and combination of pulmonary fibrosis and emphysema (CPFE). Many of the current treatments fail to attenuate the severity and progression of the disease, so a better understanding of the pathogenesis of COPD is required to develop treatments that modify it. Various types of stress are now recognized as predisposing factors in the pathogenesis of COPD. There is increased evidence of the presence of autoantibodies in COPD. Oxidative stress, for example, can lead to increased levels of reactive carbonyls in the lung, which could result in the formation of carbonyl adducts in highly immunogenic and potentially destructive on “self” proteins. This establishes a correlation between autoimmunity and COPD. Recent studies show that mitochondria are involved in the innate immune response signals, which play important roles in the activation of airway inflammation induced by cigarette smoke, lung inflammation and tissue remodeling. The connection between these three elements in the pathogenesis of COPD is discussed here. Finally some therapeutic alternatives that can impact these elements are reviewed. Cell Mol Med Res. 2017;000(000):000-000 doi: https://doi.org/10.14740/cmmr17e