Targeting Molecular and Cellular Mechanisms in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airway disease (COAD) or chronic obstructive lung disease (COLD), is the leading cause of disability worldwide. It is an increasing worldwide health issue and becomes the third most important reason of mortality and the fifth commonest cause of ill health and compromised quality of life in the world by 2020. Cigarette smoking is one of the prominent causes for pathological development of COPD. In addition, alpha1-antitrypsin (AAT) deficiency is an inherited condition, which is associated with COPD. The two main peculiar features of the disease are chronic bronchitis (contraction of airways/bronchi due to inflammation) and emphysema (damage of alveolar wall). COPD is recognised by increased number of cytotoxic T-lymphocytes, neutrophils (NPHs) and alveolar macrophages (MPs) and number of inflammatory mediators like growth factors, cytokines and chemokines. In addition, reactive oxygen species (ROS) and imbalance between oxidant and antioxidant mechanisms are also involved in pathophysiological progression of inflammatory COPD. The pulmonary inflammation may also responsible for growth, progression and development of lung cancer. Plasma levels of elastolytic enzymes such as serine proteases, cathepsins and matrix metalloproteinase (MMP) are highly increased in COPD. The pulmonary inflammation leads to development of systemic inflammation and other comorbid disorders. The disease is progressive and inflammation is predominant in comparison to asthma which seems to be resistant towards corticosteroid treatment. Specific treatment options that are working against the remodelling and inflammation need to be developed for the treatment of COPD. Hence, the present book chapter will discuss about the strategies for targeting COPD at cellular and molecular levels including their signalling pathways.