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Copyright ©ERS Journals Ltd 2003
Decreased haem oxygenase-1 and increased inducible nitric oxide synthase in the lung of severe COPD patients
1 Dept of Environmental Medicine and Public Health, 2 Dept of Clinical and Experimental Medicine, Section of Respiratory Diseases University of Padova, Padua, 3 CNR Institute of Clinical Physiology, Pisa, and 4 Dept of Medical Oncological and Radiological Sciences, Section of Respiratory Diseases, University of Modena and Reggio Emilia, Modena, Italy
CORRESPONDENCE: P. Maestrelli, Dipartimento di Medicina Ambientale e Sanitá Pubblica, Università degli Studi di Padova, via Giustiniani, 2, 35128 Padova, Italy. Fax: 39 0498212566. E-mail: piero.maestrelli@unipd.it
Keywords: cigarette smoke, immunohistochemistry, inflammation, macrophages, oxidative stress
Received: October 25, 2002
Accepted February 28, 2003
Supported by the Italian Ministry of University and Research, the University of Padova and ARCA.
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.
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