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Effect of pirfenidone on TGF-β-induced pro-fibrotic effects in primary human lung cells derived from patients with idiopathic pulmonary fibrosis

Katrin Hostettler, Jun Zhong, Michael Tamm, Didier Lardinois, Michael Roth
European Respiratory Journal 2014 44: P763; DOI:
Katrin Hostettler
1Department of BioMedicine, University Hospital Basel, Basel, Switzerland
2Clinics of Respiratory Medicine, University Hospital Basel, Basel, Switzerland
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Jun Zhong
1Department of BioMedicine, University Hospital Basel, Basel, Switzerland
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Michael Tamm
1Department of BioMedicine, University Hospital Basel, Basel, Switzerland
2Clinics of Respiratory Medicine, University Hospital Basel, Basel, Switzerland
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Didier Lardinois
3Division of Thoracic Surgery, University Hospital Basel, Basel, Switzerland
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Michael Roth
1Department of BioMedicine, University Hospital Basel, Basel, Switzerland
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Abstract

Introduction: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with poor prognosis. Pirfenidone is an orally administered pyridine that exhibits anti-fibrotic, anti-oxidant, and anti-inflammatory effects. In patients with mild-to-moderate IPF pirfenidone slowed down the decline in vital capacity and prolonged the progression-free survival. The inhibition of transforming growth factor-beta (TGF-β)-induced effects has been suggested to be part of pirfenidone's anti-fibrotic properties.

Aim: To determine the in vitro effect of pirfenidone on TGF-β1-stimulated primary human lung myofibroblasts and primary human alveolar epithelial type II cells.

Methods: Primary human myofibroblasts and alveolar epithelial type II cells were isolated from lung parenchyma derived from patients with IPF and from non-fibrotic control lungs. After incubation with pirfenidone and stimulation with TGF-β1, myofibroblast proliferation was assessed by automatic cell counting, and the effect on TGF-β1-induced epithelial-mesenchymal transition (EMT) of alveolar epithelial cells was studied.

Results: In IPF myofibroblasts, pirfenidone (1 – 4 mM) dose-dependently prevented the pro-proliferative effect of TGF-β1 (1 ng/ml). TGF-β1 caused EMT in alveolar epithelial cells as demonstrated by morphologic changes, up-regulation of fibronectin and loss of E-cadherin expression, and these effects were partly prevented by pirfenidone (4 mM).

Conclusion: Our data demonstrate that pirfenidone counteracts TGF-β-induced pro-fibrotic effects, and suggest that the inhibition of EMT may account in part for the drug's documented clinically beneficial effect.

  • Idiopathic pulmonary fibrosis
  • Epithelial cell
  • © 2014 ERS
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Effect of pirfenidone on TGF-β-induced pro-fibrotic effects in primary human lung cells derived from patients with idiopathic pulmonary fibrosis
Katrin Hostettler, Jun Zhong, Michael Tamm, Didier Lardinois, Michael Roth
European Respiratory Journal Sep 2014, 44 (Suppl 58) P763;

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Effect of pirfenidone on TGF-β-induced pro-fibrotic effects in primary human lung cells derived from patients with idiopathic pulmonary fibrosis
Katrin Hostettler, Jun Zhong, Michael Tamm, Didier Lardinois, Michael Roth
European Respiratory Journal Sep 2014, 44 (Suppl 58) P763;
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