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

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

CORRESPONDENCE: U. Costabel, Dept of Pneumology and Allergology, Ruhrlandklinik, Tüschener Weg 40, 45239 Essen, Germany. Fax: 49 2014332009. E-mail: ulrich.costabel{at}ruhrlandklinik.de

Keywords: Alveolar macrophage, cytokine, haem oxygenase-1, interstitial lung disease

Received: September 24, 2007
Accepted January 4, 2008

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

HO-1 expression in alveolar macrophages from bronchoalveolar lavage was investigated 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 semiquantitatively from 0–3 according to increasing intensity. The mean score of 100 macrophages was calculated. Macrophages were cultured and levels of interleukin (IL)-12 and IL-18 in the culture supernatants were measured by ELISA.

The mean score of HO-1 was significantly lower in IPF (67) than in sarcoidosis (105), HP (106) or controls (106). There was no significant difference between sarcoidosis, HP and controls. The score of HO-1 correlated positively with the lymphocyte percentage 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 in IPF.

The expression of haem oxygenase-1, a critical defender against oxidative stress, is decreased in macrophages of idiopathic pulmonary fibrosis patients compared with those with granulomatous lung disorders. This supports the hypothesis of an oxidant–antioxidant imbalance in the pathogenesis of idiopathic pulmonary fibrosis.