Requirement of tumour necrosis factor for development of silica-induced pulmonary fibrosis

Piguet, P F; Collart, Martine A.; Grau, Georges E.; Sappino, André-P.; Vassalli, Pierre

doi:10.1038/344245a0

Cited by 556 publications

(330 citation statements)

References 19 publications

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“…As shown by studies performed in experimental models [5] or in patients with CWP [6,24], macrophages and their products, especially TNF, appear to play a key role in the development of CWP. So we studied, in vitro, the effects of AM supernatants on the expression of adhesion molecules by two different cell types: EC, and alveolar epithelial cells.…”

Section: In Vitro Expression Of Leucocyte-endothelial Cell Adhesion Mmentioning

confidence: 99%

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Expression of leucocyte–endothelial adhesion molecules is limited to intercellular adhesion molecule-1 (ICAM-1) in the lung of pneumoconiotic patients: role of tumour necrosis factor-alpha (TNF-α)

Vanhée

Molet

Gosset

et al. 1996

Clinical and Experimental Immunology

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SUMMARYCoal workers' pneumoconiosis (CWP) is characterized by a chronic inflammatory lung reaction associated with macrophage accumulation in alveolar spaces. In this study, we investigated in CWP the implication of adhesion molecules such as E-selectin, ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1) and the role of TNF-® which is one of the cytokines inducing their expression. Adhesion molecule expression was analysed by immunohistochemistry on lung biopsies from patients with CWP and from healthy subjects. In parallel, soluble adhesion molecules were detected in bronchoalveolar lavage fluids (BALF) from patients by specific ELISA. The involvement of TNF in the induction of these adhesion molecules was measured (i) by immunohistochemistry on sections from lung fragments, and (ii) by evaluating in vitro the expression of adhesion molecules on endothelial cells and on alveolar epithelial cells in the presence of alveolar macrophage supernatants. In control subjects, a weak staining of ICAM-1 was detected only in alveolar walls, while E-selectin and VCAM-1 were undetectable. In pneumoconiotic patients, ICAM-1 was expressed at a high level by endothelium, by alveolar and bronchial epithelial cells and by alveolar macrophages. E-selectin and VCAM-1 expression remained undetectable. Measurement of soluble adhesion molecule showed that only the concentration of sICAM-1 was significantly increased in BALF from patients with CWP compared with controls. The involvement of TNF in this ICAM-1 expression was shown by the in vitro effect of alveolar macrophage supernatants on adhesion molecule expresssion by endothelial cells and epithelial cells (this effect was neutralized by anti-TNF antibodies) and by the increased production of TNF in the lung of pneumoconiotic patients. These data provide evidence for the involvement of ICAM-1, induced at least in part by alveolar macrophage-derived TNF, in the development of the inflammatory reaction in CWP.

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Section: In Vitro Expression Of Leucocyte-endothelial Cell Adhesion Mmentioning

confidence: 99%

“…Among them, TNF-is thought to be the main cytokine responsible for the development of pneumoconiotic lesions [2,5,6].…”

Section: Introductionmentioning

confidence: 99%

Expression of leucocyte–endothelial adhesion molecules is limited to intercellular adhesion molecule-1 (ICAM-1) in the lung of pneumoconiotic patients: role of tumour necrosis factor-alpha (TNF-α)

Vanhée

Molet

Gosset

et al. 1996

Clinical and Experimental Immunology

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“…Studies by Piguet and coworkers (48,49) demonstrated that TNF␣ antagonists can significantly reduce the accumulation of ECM in mouse models of silica-and bleomycin-induced pulmonary fibrosis. Silica and bleomycin stimulate the expression of TNF␣ and lead to a patchy fibrosis after 15 days.…”

Section: Tnf␣ In Fibrotic Diseases 2231mentioning

confidence: 99%

“…Treatment of established fibrosis with soluble TNFRI was also effective, as demonstrated by experiments in which soluble TNFRI was administered 25 days after bleomycin and silica. Accordingly, continuous infusion of recombinant TNF␣ strongly augmented the fibrotic process (48).…”

Section: Tnf␣ In Fibrotic Diseases 2231mentioning

confidence: 99%

The controversial role of tumor necrosis factor α in fibrotic diseases

Distler

Schett

Distler

2008

Arthritis & Rheumatism

102

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“…TNF-a has been implicated in the pathogenesis of asthma [1] and interstitial lung diseases [2]. It also plays an important role in both protective [3] and pathological immune responses to Gram-negative bacteria and mycobacteria [4].…”

mentioning

confidence: 99%

Tumour necrosis factor-alpha production in human alveolar macrophages: modulation by inhaled corticosteroid

Marshall¹,

Wangoo²,

Harrison³

et al. 2000

Eur Respir J

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Using an ex vivo alveolar macrophage model, the hypothesis that inhaled preparations of corticosteroids might have important anti-inflammatory effects on cells of the peripheral airway was tested.The tumour necrosis factor (TNF)-a-inducing potential of three glycolipid preparations from nonpathogenic (arabinofuranasyl lipoarabinomannan (LAM (Ara-LAM)) and virulent (mannase LAM (ManLAM)) mycobacteria and Gram-negative bacteria (lipopolysaccharide (LPS)), in primary alveolar macrophage preparations was investigated. A novel inhaled chlorofluorocarbon (CFC)-free preparation of beclomethasone dipropionate (hydrofluoroalkane 134a (HFA)-BDP) with increased peripheral lung deposition was investigated for its ability to modulate glycolipidinduced TNF-a production by human alveolar macrophages, in comparison with a CFC-containing preparation and placebo.Compared to the basal TNF-a bioactivity of 0.72 ng . mL -1 (geometric mean), the TNF-a bioactivity in the macrophage preparation increased following incubation with LPS (138 ng . mL -1 , p<0.001), AraLAM (12.6 ng . mL -1 , p<0.001) and ManLAM (1.42 ng . mL -1 , p=0.02). HFA-BDP, administered in vivo, significantly reduced LPS-and ManLAM-induced TNF-a production by alveolar macrophages cultured ex vivo. No change in glycolipid-induced TNF-a production was observed following in vivo administration of CFC-BDP or HFA-placebo. This is the first demonstration of an immunomodulatory effect on alveolar cells of corticosteroid delivered via metered dose inhaler. The present findings suggest that alveolar deposition of beclomethasone dipropionate is capable of modulating the inflammatory potential of the alveolar macrophage population. Eur Respir J 2000; 15: 764±770.

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Requirement of tumour necrosis factor for development of silica-induced pulmonary fibrosis

Cited by 556 publications

References 19 publications

Expression of leucocyte–endothelial adhesion molecules is limited to intercellular adhesion molecule-1 (ICAM-1) in the lung of pneumoconiotic patients: role of tumour necrosis factor-alpha (TNF-α)

Expression of leucocyte–endothelial adhesion molecules is limited to intercellular adhesion molecule-1 (ICAM-1) in the lung of pneumoconiotic patients: role of tumour necrosis factor-alpha (TNF-α)

The controversial role of tumor necrosis factor α in fibrotic diseases

Tumour necrosis factor-alpha production in human alveolar macrophages: modulation by inhaled corticosteroid

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