Intensive Care Unit, 1st Department of Respiratory Medicine, Medical School, National and Kapodistrian University of Athens and Sotiria Chest Disease Hospital, 152 Mesogeion Avenue, 11527 Athens, Greece.
Mediators Inflamm. 2013;2013:413735. doi: 10.1155/2013/413735. Epub 2013 Jul 15.
Increasing evidence indicates that chronic inflammatory and immune responses play key roles in the development and progression of COPD. Recent data provide evidence for a role in the NLRP3 inflammasome in the airway inflammation observed in COPD. Cigarette smoke activates innate immune cells by triggering pattern recognition receptors (PRRs) to release "danger signal". These signals act as ligands to Toll-like receptors (TLRs), triggering the production of cytokines and inducing innate inflammation. In smokers who develop COPD there appears to be a specific pattern of inflammation in the airways and parenchyma as a result of both innate and adaptive immune responses, with the predominance of CD8+ and CD4+ cells, and in the more severe disease, with the presence of lymphoid follicles containing B lymphocytes and T cells. Furthermore, viral and bacterial infections interfere with the chronic inflammation seen in stable COPD and exacerbations via pathogen-associated molecular patterns (PAMPs). Finally, autoimmunity is another novel aspect that may play a critical role in the pathogenesis of COPD. This review is un update of the currently discussed roles of inflammatory and immune responses in the pathogenesis of COPD.
越来越多的证据表明，慢性炎症和免疫反应在 COPD 的发生和发展中起着关键作用。最近的数据为 NLRP3 炎性小体在 COPD 中观察到的气道炎症中发挥作用提供了证据。香烟烟雾通过触发模式识别受体 (PRRs) 激活先天免疫细胞，释放“危险信号”。这些信号作为配体与 Toll 样受体 (TLRs) 结合，触发细胞因子的产生，并诱导先天炎症。在发展为 COPD 的吸烟者中，由于先天和适应性免疫反应，气道和实质中似乎存在特定的炎症模式，以 CD8+和 CD4+细胞为主，在更严重的疾病中，存在含有 B 淋巴细胞和 T 细胞的淋巴滤泡。此外，病毒和细菌感染通过病原体相关分子模式 (PAMPs) 干扰稳定 COPD 中以及加重期的慢性炎症。最后，自身免疫是另一个可能在 COPD 发病机制中起关键作用的新方面。这篇综述是对目前讨论的炎症和免疫反应在 COPD 发病机制中的作用的更新。
