Pleural Fibrosis

Jantz, Michael A.; Antony, Veena B.

doi:10.1016/j.ccm.2005.12.003

Cited by 69 publications

(52 citation statements)

References 90 publications

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“…The majority of pleural inflammatory processes resolves with treatment of the underlying cause or improves spontaneously. However, sometimes chronic scarring and fibrosis develops despite obvious resolution of the inflammatory phase (1). Progressive scarring can also occur without major inflammation, such as after surgical thoracotomy for coronary bypass (25).…”

Section: Discussionmentioning

confidence: 99%

“…It is usually considered as a complication of other disorders involving the chest cavity. Pneumonia, with parapneumonic effusion and empyema, tuberculosis and asbestos are among the most common causes for pleural fibrosis (1). Furthermore, numerous drugs can contribute to the development of pleural fibrosis, the best known being ergot drugs, cytostatic agents, and thoracic irradiation (Refs.…”

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confidence: 99%

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TGF-β1 Induces Progressive Pleural Scarring and Subpleural Fibrosis

Decologne

Kolb

Margetts

et al. 2007

The Journal of Immunology

118

119

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Pleural fibrosis is a misunderstood disorder which can cause severe restrictive lung disease with high morbidity and even mortality. The condition can develop in response to a large variety of diseases and tissue injury, among them infectious disease, asbestos, drugs, and radiation therapy. There is no efficient treatment to reverse established pleural fibrosis. TGF-β1 is suspected, even if not proven, as a key cytokine in this process. In this study, we used adenoviral gene transfer of TGF-β1 to the pleural mesothelium in rats. We show that local and transient TGF-β1 overexpression induces homogenous, prolonged, and progressive pleural fibrosis without pleurodesis, associated with severe impairment of pulmonary function. We further demonstrate that pleural fibrosis can expand into the lung parenchyma from the visceral layer, but not into the muscle from the parietal layer. We provide evidence that matrix accumulation and fibrosis within the parenchyma evolved through a process involving “mesothelial-fibroblastoid transformation” and suggest that the pleural mesothelial cell may be an important player involved in the development of the subpleural distribution pattern known to be a hallmark of pulmonary fibrosis. This new model of pleural fibrosis will allow us to better understand the mechanisms of progressive fibrogenesis, and to explore novel antifibrotic therapies in the pleural cavity.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

TGF-β1 Induces Progressive Pleural Scarring and Subpleural Fibrosis

Decologne

Kolb

Margetts

et al. 2007

The Journal of Immunology

118

119

View full text Add to dashboard Cite

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“…Along these lines, PF can result from pneumonia with complicated parapneumonic pleural effusions, empyema, trauma, malignant pleural effusions that loculate, or asbestos-related pleural injury and occur in some patients that have undergone coronary artery bypass graft surgery (12,21). PF also contributes to increased mortality of patients with comorbidities including cardiac disease (4,7). Fibrosing pleuritis is characterized by infiltration of the pleural space by proliferating, ␣-smooth muscle actin (␣-SMA)-expressing myofibroblasts.…”

mentioning

confidence: 99%

Mesomesenchymal transition of pleural mesothelial cells is PI3K and NF-κB dependent

Owens

Jeffers

Boren

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Pleural organization follows acute injury and is characterized by pleural fibrosis, which may involve the visceral and parietal pleural surfaces. This process affects patients with complicated parapneumonic pleural effusions, empyema, and other pleural diseases prone to pleural fibrosis and loculation. Pleural mesothelial cells (PMCs) undergo a process called mesothelial mesenchymal transition (MesoMT), by which PMCs acquire a profibrotic phenotype characterized by cellular enlargement and elongation, increased expression of α-smooth muscle actin (α-SMA), and matrix proteins including collagen-1. Although MesoMT contributes to pleural fibrosis and lung restriction in mice with carbon black/bleomycin-induced pleural injury and procoagulants and fibrinolytic proteases strongly induce MesoMT in vitro, the mechanism by which this transition occurs remains unclear. We found that thrombin and plasmin potently induce MesoMT in vitro as does TGF-β. Furthermore, these mediators of MesoMT activate phosphatidylinositol-3-kinase (PI3K)/Akt and NF-κB signaling pathways. Inhibition of PI3K/Akt signaling prevented TGF-β-, thrombin-, and plasmin-mediated induction of the MesoMT phenotype exhibited by primary human PMCs. Similar effects were demonstrated through blockade of the NF-κB signaling cascade using two distinctly different NF-κB inhibitors, SN50 and Bay-11 7085. Conversely, expression of constitutively active Akt-induced mesenchymal transition in human PMCs whereas the process was blocked by PX866 and AKT8. Furthermore, thrombin-mediated MesoMT is dependent on PAR-1 expression, which is linked to PI3K/Akt signaling downstream. These are the first studies to demonstrate that PI3K/Akt and/or NF-κB signaling is critical for induction of MesoMT.

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“…Pleural fibrosis as a disease entity is not as well recognised as pulmonary fibrosis but, nevertheless, it can cause severe functional impairment and markedly reduce quality of life. The initiating events for pleural fibrosis are often identifiable and include drugs, radiation, asbestos, haemothorax, thoracotomy for coronary bypass and, most often, infectious diseases [1]. This is in strong contrast to idiopathic pulmonary fibrosis (IPF), which has no underlying cause.…”

mentioning

confidence: 99%

Bleomycin induces pleural and subpleural fibrosis in the presence of carbon particles

Decologne¹,

Wettstein²,

Kolb³

et al. 2009

Eur Respir J

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The pathological changes in idiopathic pulmonary fibrosis (IPF) typically start in subpleural lung regions, a feature that is currently not explained. IPF, as well as bleomycininduced lung fibrosis, are more common in smokers. We hypothesised that carbon particles, which are major components of cigarette smoke that are transported to alveoli and pleural surface, might be involved in the development of subpleural fibrosis through interaction with pleural mesothelial cells.Carbon particles were administered to mice in combination with bleomycin through intratracheal and/or intrapleural injection and fibrosis was assessed using histomorphometry.Carbon administered to the chest cavity caused severe pleural fibrosis in the presence of bleomycin, whereas bleomycin alone had no fibrogenic effect. The pleural response was associated with progressive fibrosis in subpleural regions, similar to IPF in humans. Matrix accumulation within this area evolved through mesothelial-fibroblastoid transformation, where mesothelial cells acquire myofibroblast characteristics. In contrast, carbon did not exaggerate bleomycin-induced pulmonary fibrosis after combined intratracheal administration.This represents a novel approach to induce a robust experimental model of pleural fibrosis. It also suggests that carbon particles might be involved as a cofactor in the initiation and/or progression of (subpleural) pulmonary and pleural fibrosis. Mesothelial cells appear to be critical contributors to this fibrotic process.

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Pleural Fibrosis

Cited by 69 publications

References 90 publications

TGF-β1 Induces Progressive Pleural Scarring and Subpleural Fibrosis

TGF-β1 Induces Progressive Pleural Scarring and Subpleural Fibrosis

Mesomesenchymal transition of pleural mesothelial cells is PI3K and NF-κB dependent

Bleomycin induces pleural and subpleural fibrosis in the presence of carbon particles

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