Oxidized BAL fluid proteins in patients with interstitial lung diseases

Lenz, Anke‐Gabriele; Costabel, Ulrich; Maier, K.L

doi:10.1183/09031936.96.09020307

Cited by 103 publications

(79 citation statements)

References 36 publications

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“…Oxidative modification of mitochondrial DNA has been observed in lung epithelial cells of IPF patients [5]. Oxidised BALF proteins, characterised by oxidation of methionine residues or carbonylation, are increased in patients with IPF [6,7]. There is also an increase in 8-isoprostane, a biomarker of oxidative stress, in the BALF of IPF patients [8].…”

mentioning

confidence: 72%

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

Dalavanga²,

Poulakis³

et al. 2008

Eur Respir J

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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.

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confidence: 72%

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

Dalavanga²,

Poulakis³

et al. 2008

Eur Respir J

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“…The role of ROS in the development of lung fibrosis has already been reported in a large number of pathological conditions, such as bronchopulmonary dysplasia in pre-term infants [20], adult respiratory distress syndrome [21,22], sarcoidosis [23], idiopathic pulmonary fibrosis [24], and in the animal models of silicosis and asbestos-induced pulmonary fibrosis [25,26]. The most relevant model demonstrating the role of ROS in lung fibrosis is certainly the murine model of lung fibrosis induced by intratracheal instillation of bleomycin.…”

Section: Discussionmentioning

confidence: 99%

The oxidation induced by antimyeloperoxidase antibodies triggers fibrosis in microscopic polyangiitis

Guilpain¹,

Chéreau²,

Goulvestre³

et al. 2010

Eur Respir J

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Lung fibrosis is considered a severe manifestation of microscopic polyangiitis (MPA). Antimyeloperoxidase (anti-MPO) antibodies in MPA patients' sera can activate MPO and lead to the production of reactive oxygen species (ROS). While high levels of ROS are cytotoxic, low levels can induce fibroblast proliferation. Therefore, we hypothesised that the oxidative stress induced by anti-MPO antibodies could contribute to lung fibrosis.24 MPA patients (45 sera) were enrolled in the study, including nine patients (22 sera) with lung fibrosis. Serum advanced oxidation protein products (AOPP), MPO-induced hypochlorous acid (HOCl) and serum-induced fibroblast proliferation were assayed.AOPP levels, MPO-induced HOCl production and serum-induced fibroblast proliferation were higher in patients than in healthy controls (p,0.0001, p50.0001 and p50.0005, respectively). Increased HOCl production was associated with active disease (p50.002). Serum AOPP levels and serum-induced fibroblast proliferation were higher in patients with active MPA and lung fibrosis (p,0.0001). A significant linear relationship between fibroblast proliferation, AOPP levels and HOCl production was observed only in patients with lung fibrosis.Oxidative stress, in particular the production of HOCl through the interaction of MPO with anti-MPO antibodies, could trigger the fibrotic process observed in MPA.

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“…2 Either directly or via formation of intermediate lipid or protein peroxidation products, they may enhance inflammation by activation of stress kinases and redox-sensitive transcription factors such as NF-kappa B and AP-1. 3 Previously, it was shown that reactive oxygen species such as superoxide, hydrogen peroxide, and hydroxyl radicals contribute to inflammatory injury in adult patients with asthma, 4,5 chronic bronchitis, 6 interstitial lung disease (ILD), 7 or cystic fibrosis. 8 High levels of free radicals are produced in the lungs by activated inflammatory cells, i.e., neutrophils, eosinophils, and alveolar macrophages.…”

Section: Introductionmentioning

confidence: 99%

Protein Oxidation by Chronic Pulmonary Diseases in Children

Starosta

Griese

2005

Pediatric Pulmonology

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Summary. The oxidation of proteins may play an important role in the pathogenesis of chronic inflammatory lung diseases, and may contribute to lung damage. However, the extent of oxidation and the distribution among proteins are not known for most pediatric lung diseases. In this work, protein oxidation was assessed as protein carbonyls. Bronchoalveolar lavages (BAL) from children with chronic lung diseases were investigated by dot-blot assay for content and for pattern of distribution of oxidized proteins by two-dimensional (2D) electrophoresis and Western blotting. Significantly higher levels of protein oxidation than in healthy controls were determined in groups of patients with interstitial lung disease, gastro-esophageal reflux disease, and pulmonary alveolar proteinosis. The proteins most sensitive to oxidation were serum albumin, surfactant protein A, and a1-antitrypsin. Our data show increased oxidative stress in lungs of children with chronic pulmonary diseases, with significant interindividual variations. The extent of protein oxidation was proportional to the count of neutrophilic granulocytes in BAL fluid. These findings strongly support the concept that an abundance of reactive oxygen species produced during neutrophilic inflammation may be a deleterious factor, leading to pulmonary damage in these patients.

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Oxidized BAL fluid proteins in patients with interstitial lung diseases

Cited by 103 publications

References 36 publications

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

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

The oxidation induced by antimyeloperoxidase antibodies triggers fibrosis in microscopic polyangiitis

Protein Oxidation by Chronic Pulmonary Diseases in Children

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