Maestrelli P, El Messlemani A H, De Fina O, Nowicki Y, Saetta M, Mapp C, Fabbri L M
Department of Environmental Medicine and Public Health, University of Padua, Padua, Italy.
Am J Respir Crit Care Med. 2001 Oct 15;164(8 Pt 1):1508-13. doi: 10.1164/ajrccm.164.8.2011083.
It has been suggested that oxidative stress protein heme oxygenase (HO)-1 plays a role in chronic airway diseases including chronic obstructive pulmonary disease (COPD). The inducible isoform HO-1 and the constitutive HO-2 catalyze the same reaction. Their distribution in situ was studied in lungs of 10 nonsmoking subjects, 6 healthy smokers, and 10 smokers with COPD. Paraffin-embedded sections of surgical lung specimens were immunostained with antibodies against HO-1 and HO-2. HO-1 immunoreactivity was observed mainly in alveolar macrophages. HO-1-positive macrophages were increased in smokers with COPD (median: 36%) as compared with nonsmoking subjects (13%; p < 0.02), whereas no differences were observed between patients with COPD and healthy smokers (34%). HO-2 had a more widespread distribution in cells of the alveolar wall, in adventitia of pulmonary arteries and bronchioles, and in vascular smooth muscle. Lower percentages of alveolar macrophages exhibited positive staining for HO-2 without significant differences between the three groups. HO-2(+) cells in the alveolar wall were increased in smokers with (15/mm) and without COPD (12/mm) as compared with nonsmokers (8/mm, p < 0.01). In conclusion, inducible HO-1 and constitutive HO-2 are detectable in human lung tissue and their expression is increased in smokers, suggesting that oxidative stress due to cigarette smoke may increase lung cells expressing HO-1 and HO-2.
有人提出，氧化应激蛋白血红素加氧酶（HO）-1在包括慢性阻塞性肺疾病（COPD）在内的慢性气道疾病中起作用。诱导型同工型HO-1和组成型HO-2催化相同的反应。在10名非吸烟受试者、6名健康吸烟者和10名患有COPD的吸烟者的肺中研究了它们的原位分布。手术肺标本的石蜡包埋切片用抗HO-1和HO-2的抗体进行免疫染色。HO-1免疫反应性主要在肺泡巨噬细胞中观察到。与非吸烟受试者（13%；p<0.02）相比，患有COPD的吸烟者中HO-1阳性巨噬细胞增加（中位数：36%），而COPD患者与健康吸烟者（34%）之间未观察到差异。HO-2在肺泡壁细胞、肺动脉和细支气管外膜以及血管平滑肌中分布更广泛。较低百分比的肺泡巨噬细胞对HO-2呈阳性染色，三组之间无显著差异。与非吸烟者（8/mm，p<0.01）相比，患有（15/mm）和未患有COPD（12/mm）的吸烟者肺泡壁中的HO-2（+）细胞增加。总之，在人肺组织中可检测到诱导型HO-1和组成型HO-2，并且它们在吸烟者中的表达增加，这表明香烟烟雾引起的氧化应激可能增加表达HO-1和HO-2的肺细胞。
