Inflammatory Diseases of the Lung Induced by Conventional Cigarette Smoke A Review
Inflammatory Diseases of the Lung Induced by Conventional Cigarette Smoke A Review
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DOI：
10.1378/chest.15-0409
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发表时间：
2015-11-01
期刊：
影响因子：
9.6
通讯作者：
Hwang, John H.
中科院分区：
文献类型：
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作者：
Alexander, Laura E. Crotty;Shin, Stephanie;Hwang, John H.
在20世纪之前，吸烟引起的肺部疾病极为罕见。随着机器卷烟的商业化和引进，世界范围内的使用量急剧上升，一些新的肺部疾病已经得到确认。大多数由吸烟引起的肺部疾病（CS）起源于炎症。气道上皮细胞和肺泡巨噬细胞对CS的反应改变了炎症信号，导致淋巴细胞、嗜酸性粒细胞、中性粒细胞和肥大细胞聚集到肺部，这取决于信号通路（核因子κ B、单磷酸腺苷活化蛋白激酶、c-Jun n -末端激酶、p38、信号转导和转录激活因子3）的激活。在CS暴露下，多种蛋白质被上调和分泌，其中许多具有免疫调节活性，有助于疾病的发病机制。特别是，金属蛋白酶9和12、表面活性剂蛋白D、抗菌肽（LL-37和人β防御素2）、IL-1、IL-6、IL-8和IL-17在持续炎症的吸烟者肺部中含量较高。然而，吸烟引起的炎症性疾病的许多潜在机制尚不清楚。我们在此综述了已知的cs诱导疾病的细胞和分子机制，包括慢性阻塞性肺病、呼吸性细支气管炎-间质性肺病、脱屑性间质性肺炎、急性嗜酸性肺炎、慢性鼻窦炎、肺朗格汉斯细胞组织细胞增多症和慢性细菌感染。我们还讨论了二手和三手烟暴露引起的炎症以及由此导致的肺部疾病。新的靶向抗炎治疗方案目前正在研究中，有望在治疗这些高度流行的吸烟引起的疾病方面产生有希望的结果。
Smoking-induced lung diseases were extremely rare prior to the 20th century. With commercialization and introduction of machine-made cigarettes, worldwide use skyrocketed and several new pulmonary diseases have been recognized. The majority of pulmonary diseases caused by cigarette smoke (CS) are inflammatory in origin. Airway epithelial cells and alveolar macrophages have altered inflammatory signaling in response to CS, which leads to recruitment of lymphocytes, eosinophils, neutrophils, and mast cells to the lungs-depending on the signaling pathway (nuclear factor-kappa B, adenosine monophosphate-activated protein kinase, c-Jun N-terminal kinase, p38, and signal transducer and activator of transcription 3) activated. Multiple proteins are upregulated and secreted in response to CS exposure, and many of these have immunomodulatory activities that contribute to disease pathogenesis. In particular, metalloproteases 9 and 12, surfactant protein D, antimicrobial peptides (LL-37 and human beta defensin 2), and IL-1, IL-6, IL-8, and IL-17 have been found in higher quantities in the lungs of smokers with ongoing inflammation. However, many underlying mechanisms of smoking-induced inflammatory diseases are not yet known. We review here the known cellular and molecular mechanisms of CS-induced diseases, including COPD, respiratory bronchiolitis-interstitial lung disease, desquamative interstitial pneumonia, acute eosinophilic pneumonia, chronic rhinosinusitis, pulmonary Langerhans cell histiocytosis, and chronic bacterial infections. We also discuss inflammation induced by secondhand and thirdhand smoke exposure and the pulmonary diseases that result. New targeted antiinflammatory therapeutic options are currently under investigation and hopefully will yield promising results for the treatment of these highly prevalent smoking-induced diseases.