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• W2034867905 abstract "Chronic obstructive pulmonary disease (COPD) is a major public health problem because of its high prevalence, rising incidence and associated socio-economic cost. The inhalation of toxic particles and gases, mostly tobacco smoke, is the main risk factor for COPD. Yet, not all smokers are equally susceptible to these toxic effects and only a percentage of them develop the disease (so-called ‘susceptible smokers’). This, in combination with the observation that COPD shows familial aggregation, suggests that the genetic background of the smoker is a key element in the pathogenesis of the disease. On the other hand, it is well established that ‘susceptible’ smokers exhibit an enhanced inflammatory response of the lung parenchyma as compared with ‘resistant’ smokers (i.e., those who manage to maintain lung function within the normal age range despite their habit). Importantly, in COPD patients this inflammatory response does not resolve after quitting smoking, again at variance with resistant smokers. All in all, these observations suggest that the pathogenesis of COPD may involve, in some patients, an autoimmune component which contributes to the enhanced and persistent inflammatory response that characterizes the disease. Here we: i) review briefly the pathobiology of COPD; ii) present the available scientific evidence supporting a potential role for autoimmunity in COPD; iii) propose a three-step pathogenic hypothesis in the transition from smoking to COPD; and iv) discuss potential implications for the diagnosis and treatment of this frequent, growing, devastating and costly disease." @default.
• W2034867905 created "2016-06-24" @default.
• W2034867905 creator A5054165025 @default.
• W2034867905 creator A5056342735 @default.
• W2034867905 creator A5083167610 @default.
• W2034867905 date "2013-09-01" @default.
• W2034867905 modified "2023-10-14" @default.
• W2034867905 title "Immune response in chronic obstructive pulmonary disease" @default.
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