Department of Critical Care Medicine and Pulmonary Services, Evangelismos General Hospital, Ipsilantou Str 45-7, Athens 10675, Greece.
Curr Drug Targets. 2011 Apr;12(4):450-9. doi: 10.2174/138945011794751546.
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 of the 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.
吸烟者的肺部会接触到香烟烟雾中的有毒物质，但只有 10-20%的人会发展为慢性阻塞性肺疾病（COPD）。为了使 COPD 发展，香烟烟雾必须绕过或超过宿主的第一道防线，即呼吸道黏膜上皮，它作为一种有效的物理屏障和先天免疫系统，提供即时但非特异性的反应。在这篇综述中，我们将简要描述香烟烟雾如何成功地损害黏膜上皮的物理屏障和先天免疫系统，以及它如何诱导适应性免疫系统的效应机制，这些机制对宿主具有特别的细胞毒性。我们还将讨论其他具有免疫原性潜力的刺激物的作用，如定植或逃避 COPD 患者肺部的病原体以及自身组织抗原的作用，当发生慢性炎症时，可能导致自身免疫性疾病。尽管 COPD 中不良的先天和适应性免疫反应的主要机制仍存在争议，但目前人们普遍认为它们是 COPD 的根本原因。
