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

Ye, Q; Dalavanga, Yotanna; Poulakis, N.; Sixt, Stephan Urs; Guzman, Josune; Costabel, Ulrich

doi:10.1183/09031936.00125407

Cited by 38 publications

(28 citation statements)

References 39 publications

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“…A pathogenic role for macrophages in pulmonary fibrosis has been postulated for many years, and described mechanisms have included overexpression of reactive oxygen species [147-151], proteinase-activated receptors [152-154], Fas ligand [155], and profibrotic cytokines [97,154,156-162]. …”

Section: Reviewmentioning

confidence: 99%

Molecular and cellular mechanisms of pulmonary fibrosis

Todd

Luzina

Atamas

2012

Fibrogenesis Tissue Repair

356

293

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Pulmonary fibrosis is a chronic lung disease characterized by excessive accumulation of extracellular matrix (ECM) and remodeling of the lung architecture. Idiopathic pulmonary fibrosis is considered the most common and severe form of the disease, with a median survival of approximately three years and no proven effective therapy. Despite the fact that effective treatments are absent and the precise mechanisms that drive fibrosis in most patients remain incompletely understood, an extensive body of scientific literature regarding pulmonary fibrosis has accumulated over the past 35 years. In this review, we discuss three broad areas which have been explored that may be responsible for the combination of altered lung fibroblasts, loss of alveolar epithelial cells, and excessive accumulation of ECM: inflammation and immune mechanisms, oxidative stress and oxidative signaling, and procoagulant mechanisms. We discuss each of these processes separately to facilitate clarity, but certainly significant interplay will occur amongst these pathways in patients with this disease.

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Section: Reviewmentioning

confidence: 99%

Molecular and cellular mechanisms of pulmonary fibrosis

Todd

Luzina

Atamas

2012

Fibrogenesis Tissue Repair

356

293

View full text Add to dashboard Cite

show abstract

“…In patients with IPF there is an increase in oxidative damage and an increase in exhaled nitric oxide levels (Saleh et al, 1997;Paredi et al, 1999;Pullamsetti et al, 2011). Fibroblasts from IPF patients exhibit decreased nuclear Nrf-2 expression, and IPF patients have shown diminished antioxidative capacity by having decreased expression of Nrf-2 target genes and decreased levels of glutathione (Beeh et al, 2002;Peltoniemi et al, 2004;Vuorinen et al, 2008;Ye et al, 2008;Artaud-Macari et al, 2013). In addition, preclinical models show that mice with a genetic deletion of Nrf-2 have decreased survival and increased inflammation following BLM-induced damage (Kikuchi et al, 2010).…”

Section: Spl-334 Attenuates Inflammation and Fibrosis In The Lungsmentioning

confidence: 99%

Pharmacological In Vivo Inhibition of S-Nitrosoglutathione Reductase Attenuates Bleomycin-Induced Inflammation and Fibrosis

Luzina

Lockatell

Todd

et al. 2015

The Journal of Pharmacology and Experimental Therapeutics

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Interstitial lung disease (ILD) characterized by pulmonary fibrosis and inflammation poses a substantial biomedical challenge due to often negative disease outcomes combined with the need to develop better, more effective therapies. We assessed the in vivo effect of administration of a pharmacological inhibitor of Snitrosoglutathione reductase, SPL-334, in a mouse model of ILD induced by intratracheal instillation of bleomycin (BLM). Daily i.p. administration of SPL-334 alone at 0.3, 1.0, or 3.0 mg/kg had no effect on animal body weight, appearance, behavior, total and differential bronchoalveolar lavage (BAL) cell counts, or collagen accumulation in the lungs, showing no toxicity of our investigational compound. Similar administration of SPL-334 for 7 days before and for an additional 14 days after BLM instillation resulted in a preventive protective effect on the BLM challenge-induced decline in total body weight and changes in total and differential BAL cellularity. In the therapeutic treatment regimen, SPL-334 was administered at days 7-21 after BLM challenge. Such treatment attenuated the BLM challenge-induced decline in total body weight, changes in total and differential BAL cellularity, and magnitudes of histologic changes and collagen accumulation in the lungs. These changes were accompanied by an attenuation of BLMinduced elevations in pulmonary levels of profibrotic cytokines interleukin-6, monocyte chemoattractant protein-1, and transforming growth factor-b (TGF-b). Experiments in cell cultures of primary normal human lung fibroblast have demonstrated attenuation of TGF-b-induced upregulation in collagen by SPL-334. It was concluded that SPL-334 is a potential therapeutic agent for ILD.

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“…In our model, these two processes appeared at different time points: at 7 days, the main manifestation was alveolitis, and then at 28 days, significant fibrosis appeared (Zheng et al, 2000;Lu et al, 2001;Ye et al, 2008). The current study identified that the model group had significant lung inflammation and fibrosis at 7 days.…”

Section: Discussionmentioning

confidence: 47%

Comparative study between Ephedra sinica Stapf and Fructus Schisandrae Chinensis on ET-1 and 6-keto-prostaglandin F1α in rats with idiopathic pulmonary fibrosis

Zhai¹,

Hhang²,

Gao³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to evaluate differences in the effects of Ephedra sinica Stapf and Fructus Schisandrae Chinensis on angiogenesis in the treatment of bleomycin-induced rat idiopathic pulmonary fibrosis. The rat models were created using bleomycin. The animals were divided into six groups: model, control, Ephedra alone, Schisandrae alone, combination of Ephedra and Schisandrae, and hydrocortisone alone. The treatments were administered for 28 days. After 7 and 28 days, the rats were sacrificed for pathological morphology examination, microvascular density determination, and angiogenesis-related cytokine examination. The Ephedra and hydrocortisone groups demonstrated significantly reduced alveolitis and pulmonary fibrosis grades compared with the model group (P < 0.05). The number of blood vessels in the Ephedra group was higher than that in the Schisandrae and combination therapy groups. At 7 days, the expression level of endothelin (ET)-1 in the model group was significantly higher than that in the normal group (P < 0.01). The level of 6-keto-prostaglandin F1α (6-keto-PGF1α) in the treatment group increased, and there were significant differences between the Ephedra group and the combination therapy and normal groups (P < 0.05). Ephedra inhibited the increase in the lung coefficient. The combination therapy prevented pulmonary artery injury and angiogenesis of the arteries by reducing the level of ET-1 and promoting the level of 6-keto-PGF1α in the blood. Ephedra and Schisandrae prevented alveolitis and the development of pulmonary fibrosis.

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

Cited by 38 publications

References 39 publications

Molecular and cellular mechanisms of pulmonary fibrosis

Molecular and cellular mechanisms of pulmonary fibrosis

Pharmacological In Vivo Inhibition of S-Nitrosoglutathione Reductase Attenuates Bleomycin-Induced Inflammation and Fibrosis

Comparative study between Ephedra sinica Stapf and Fructus Schisandrae Chinensis on ET-1 and 6-keto-prostaglandin F1α in rats with idiopathic pulmonary fibrosis

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