TY - JOUR T1 - Decreased haem oxygenase-1 and increased inducible nitric oxide synthase in the lung of severe COPD patients JF - European Respiratory Journal JO - Eur Respir J SP - 971 LP - 976 DO - 10.1183/09031936.03.00098203 VL - 21 IS - 6 AU - P. Maestrelli AU - C. Páska AU - M. Saetta AU - G. Turato AU - Y. Nowicki AU - S. Monti AU - B. Formichi AU - M. Miniati AU - L.M. Fabbri Y1 - 2003/06/01 UR - http://erj.ersjournals.com/content/21/6/971.abstract N2 - Oxidant/antioxidant imbalance is implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). The current study examined the expression of antioxidant and pro-oxidant enzymes, haem oxygenases (HO) and inducible nitric oxide synthase (iNOS) respectively, in patients with severe COPD and control smokers without lung function impairment. Immunoreactivity for HO-1, HO-2, iNOS and nitric oxide-derived oxidants expressed as nitrotyrosine (N-Tyr) was quantified in peripheral lung. HO-1+ alveolar macrophages were decreased in severe COPD compared to control smokers, whereas no difference was observed in iNOS+ macrophages. In contrast, severe patients had significantly higher numbers of iNOS+ cells in alveolar walls. These iNOS+ cells were identified as type 2 pneumocytes and their number was inversely related to HO-1+ macrophages. There were no significant differences in N-Tyr immunostaining between the two groups. However, the rate of protein nitration in lungtissue was directly related to iNOS expression and associated with lower valuesofforced expiratory volume in one second/forced vital capacity. HO-2 was constitutively expressed by type 2 pneumocytes and these cells were increased in severe COPD. In conclusion, the results suggest that the enzymes involved in the oxidative stressresponse may have a different role in the lung defence and that imbalance betweenhaemoxygenase-1 and inducible nitric oxide synthase may be associated withthe development of severe impairment in chronic obstructive pulmonary disease patients. Supported by the Italian Ministry of University and Research, the University of Padova and ARCA. ER -