Evasion of COPD in smokers: at what price?

Abstract

Investigations toward the understanding of chronic obstructive pulmonary disease (COPD) have been directed, so far, to the study of mechanisms leading to the disease. We believe that understanding why ,80% of smokers evade COPD and how this evasion is accomplished might be a fruitful endeavour that could advance knowledge of the development of the disease. Since the inflammatory infiltrate smokers develop seems to be the key element leading to the lung destruction in COPD, the understanding of the possible ways inflammation can be dampened, as well as its consequences, ought to be important. We review here some of the mechanisms by which inflammation is controlled: by the post-translational regulons, by the mechanisms preventing full activation of dendritic cells and by the regulatory T-cells. The potential role of the M2 alveolar macrophage phenotype and the newly described myeloid-derived suppressor cells is mentioned. We also point out that evasion comes at a price, as healthy smokers might be immunosuppressed to some extent and unable to prevent the development of cancer, certainly less so than in severe COPD, where immunity is heightened. Probably, the knowledge of the mechanisms of evasion from COPD could add significantly to the understanding of those leading to the disease.

Curcumin ameliorates alveolar epithelial injury in a rat model of chronic obstructive pulmonary disease

“…Cigarette smoke is commonly used to establish a rat model of COPD because smoking is the main factor in the pathogenesis of human COPD [17]. However, a majority of smokers do not develop COPD and numerous patients with COPD are never-smokers [8], indicating that COPD is a multifactorial degenerative disease. A rat model of COPD induced by a combination of cigarette smoke and LPS may be more representative for the human situation and may therefore be a preferred model to investigate the pathogenesis of COPD.…”

Is Chronic Obstructive Pulmonary Disease a Disease of Aging?

“…It is well accepted that an abnormal inflammatory response with a strong adaptive immune component is an important pathogenic factor for COPD [23,24]. However, most smokers evade the development of COPD, regardless of how much they smoke, via an active process that dampens this inflammatory response [20]. Obviously smokers that go on to develop COPD have been unable to dampen the cigarette smoke-induced inflammation.…”

“…The GOLD working group has made great efforts to classify COPD by its severity, which might imply different individual predispositions, risk factors, and abilities to dampen inflammation, promoting a total or partial evasion of COPD, as we recently discussed [20]. Can patients with COPD (previous) GOLD stages II, III, and IV be considered a single homogeneous population and be analyzed together?…”

Myeloid‑derived suppressor cells in bronchoalveolar lavage fluid in patients with chronic obstructive pulmonary disease

“…[33][34][35] MDSCs were shown to be an inherent part of chronic inflammation, so it was tempting to speculate that they may be directly involved in the chronic inflammatory process such as COPD. 13,35 There are only a few reports assessing the occurrence of circulating MDSCs in the blood of patients with COPD and only one in BALF.…”