Decreased expression of heme oxygenase-1 by alveolar macrophages in idiopathic pulmonary fibrosis

¹ Dept of Pneumology and Allergology, Ruhrlandklinik, Medical Faculty, University of Duisburg-Essen, Germany; Beijing Institute of Respiratory Medicine, Beijing Chaoyang Hospital, Capital University of Medical Sciences, Beijing, China
² Dept of Pneumology and Allergology, Ruhrlandklinik, Medical Faculty, University of Duisburg-Essen, Germany
³ Dept of Anesthesiology and Intensive Care Medicine, University of Duisburg-Essen, School of Medicine Essen
⁴ General and Experimental Pathology, Ruhr University, Bochum, Germany

^* To whom correspondence should be addressed. E-mail: ulrich.costabel{at}ruhrlandklinik.de.

	Abstract

Heme oxygenase (HO)-1 is an oxidative stress responsive protein that may be involved in the pathogenesis of interstitial lung disease.

We investigated HO-1 expression in alveolar macrophages from bronchoalveolar lavage in 24 patients with idiopathic pulmonary fibrosis (IPF), 16 with sarcoidosis, 14 with hypersensitivity pneumonitis (HP), and 13 controls. Using immunocytochemistry, HO-1 expression in macrophages was scored semi-quantitatively from 0 to 3 according to increasing intensity. The mean score of 100 macrophages was calculated. Macrophages were cultured, IL-12 and IL-18 in the culture supernatants was measured by ELISA.

The score of HO-1 was significantly lower in IPF (mean 67) than in sarcoidosis (105) or HP (106) and in controls (106). There was no significant difference between sarcoidosis, HP and controls. The score of HO-1 correlated positively with the lymphocyte percentage (r=0.38, p<0.05) in sarcoidosis and HP. Positive correlations were found between the score of HO-1 and the release of IL-12 and IL-18 by macrophages (r=0.58, p<0.05; r=0.60, p<0.05) in IPF.

The expression of HO-1, a critical defender against oxidative stress, is decreased in macrophages of IPF compared to granulomatous lung disorders. This supports the hypothesis of an oxidant-antioxidant imbalance in the pathogenesis of IPF.

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