The lungs of smokers are exposed to the toxic substances of cigarette smoke, but only 10-20% of them will develop chronic obstructive pulmonary disease (COPD). For COPD to develop, cigarette smoke has to bypass or overwhelm the host front lines of defence, i.e. the respiratory tract mucosal epithelium, which serves as an effective physical barrier and the innate immune system, which provides an immediate, yet non-specific response. In this review, we will describe briefly how cigarette smoke succeeds in damaging the physical barrier of mucosal epithelium and the innate immune system, and how it induces effector mechanisms of the adaptive immune system, which are particularly cytotoxic to the host. We will also discuss the role of other stimuli with immunogenic potential, such role of pathogens which colonize or evade the lungs of COPD patients and of self tissue antigens, which may lead to autoimmune disease when there is chronic inflammation. Although the primary mechanism(s) of undesirable innate and adaptive immune responses in COPD are still a matter of debate, it is currently accepted that they are the root cause of COPD.
Keywords: Chronic obstructive pulmonary disease, cigarette smoke, pathogenesis, innate, adaptive, epithelium, inflammation, protease, oxidative stress, lymphocyte, dendritic cell, autoimmune
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