Schlick W
Wien Med Wochenschr. 1986 Dec 31;136(23-24):610-3.
From a synopsis of the large number of epidemiological studies of the recent 20 years it is know, that inhalation of cigarette smoke is the most important factor that generates chronic bronchitis. Other noxious agents about which there are still controversial opinions, are air pollution and occupational inhalants. Although hypersecretion of mucus is the primary symptom of chronic bronchitis, it seems to have no particular prognostic meaning. Whether severe airflow obstruction develops, apparently depends upon predisposing factors such as disturbances of humoral immunity manifested by marked hypogammaglobulinemia or a defect of mucociliary clearance. In recent time increased serum IgE-levels in mom-atopic smokers with bronchial obstructions were reported. Frequent recurrent bronchial infections alone seem to be no serious risk factor. The molecular mechanisms that lead to structural damage are clarified. Activated alveolar macrophages attract polymorphonuclear leucocytes by chemotaxis. These cells set free proteolytic enzymes such as elastases. In addition certain oxidants inhibit the protection system of proteinase inhibitors.
从近20年大量流行病学研究的概要可知，吸入香烟烟雾是引发慢性支气管炎的最重要因素。其他仍存在争议的有害因素是空气污染和职业性吸入物。虽然黏液分泌过多是慢性支气管炎的主要症状，但它似乎没有特殊的预后意义。是否会出现严重的气流阻塞，显然取决于一些易感因素，如以显著低丙种球蛋白血症表现的体液免疫紊乱或黏液纤毛清除功能缺陷。最近有报道称，患有支气管阻塞的非特应性吸烟者血清IgE水平升高。仅频繁反复的支气管感染似乎并不是严重的危险因素。导致结构损伤的分子机制已得到阐明。活化的肺泡巨噬细胞通过趋化作用吸引多形核白细胞。这些细胞释放出诸如弹性蛋白酶等蛋白水解酶。此外，某些氧化剂会抑制蛋白酶抑制剂的保护系统。
