Secretion of Fibronectin by Mineral Dust-Derived Alveolar Macrophages and Activated Peritoneal Macrophages

Davies, R.; Erdogdu, G.

doi:10.3109/01902148909087859

Cited by 17 publications

(6 citation statements)

References 33 publications

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“…In vivo and in vitro studies have shown that AM plays an important role in CWP. AM arethe main target cells exposed to dust andincreased AM numbers are observed in CWP patients that correspondto excess amount of dust in the lungs [ 34 ]. Length of exposure to dust and the onset age are critical determinant factors in the incidence of CWP.…”

Section: Discussionmentioning

confidence: 99%

TNFR/TNF-α signaling pathway regulates apoptosis of alveolar macrophages in coal workers' pneumoconiosis

et al. 2017

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We explored the role of TNFR/TNF-α signalingin apoptosis among alveolar macrophages (AM) and its relevance to the development of coal workers’ pneumoconiosis (CWP). Purified alveolar macrophages (AMs) were prepared from bronchoalveolar lavage fluid harvested from 366 CWP patients and 120 healthy subjects enrolled inthe study. The purified AMs were then divided into control, SOD, anti-TNFR, TNFR and NFkB inhibitor groups and analyzed for apoptosis usingflow cytometry (sub-diploid peak) and western blotting (Bcl-2, Caspase-3 and Caspase-8 expression). We found thatAM apoptosis washigher amongCWP patients than thehealthycontrols. Expression ofBcl-2, Caspase-3 and Caspase-8 was higher inAMs from CWP patientsthan in those from the controlsand correlated with increased AM apoptosis. Univariate and multivariate analyses suggested that CWP grade, initial exposure time, exposure time inyears, and CWP onset agewereall associated with altered levels of Bcl-2, Caspase-3 and Caspase-8. Inhibition of TNFR/TNF-α signaling usinganti-TNFR antibody, SOD or NFkB inhibitionreduced AM apoptosisand decreased Bcl-2, Caspase-3 and Caspase-8 expression. These data suggestinhibition of a TNFR/TNF-α signaling pathway is a potentiallyeffective means ofalleviating CWP by inhibiting AM apoptosis.

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Section: Discussionmentioning

confidence: 99%

TNFR/TNF-α signaling pathway regulates apoptosis of alveolar macrophages in coal workers' pneumoconiosis

et al. 2017

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“…In addition to proinflammatory cytokines, numerous studies have also found factors susceptible to modify fibroblast proliferation and collagen deposition in supernatants of AMs exposed to mineral particles [30,31]. Both compact and fibrous particles induce AMs to secrete fibronectin [32][33][34], and large amounts of plateletderived growth factor (PDGF) [35][36][37], which is known as a competence factor for fibroblast proliferation [38,39].…”

Section: Alveolar Macrophage Activation and Cytokine Production After...mentioning

confidence: 99%

Cytokines and cytokine network in silicosis and coal workers' pneumoconiosis

Vanhée¹,

Gosset²,

Boitelle³

et al. 1995

Eur Respir J

145

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The alveolar macrophage (AM) is a critically important cell playing a prominent role in lung inflammation via the production of oxygen radicals, enzymes, arachidonic acid metabolites, and also a large panel of cytokines. Among interstitial lung disorders, silicosis and coal workers' pneumoconiosis (CWP) are the most widespread fibrotic lung diseases. Although their pathophysiology remains incompletely understood, several lines of evidence suggest the participation of cytokines produced by AMs at least in the initiation of the alveolitis. In vitro exposure of AMs (obtained from healthy subjects) to coal dust particles triggered a significant release of tumour necrosis factor (TNF) and interleukin-6, by comparison with titanium dioxide used as a biologically inert control dust. Moreover, it appeared that coal mine dust was more aggressive than similar concentrations of pure silica, suggesting that cytokine secretion induced by coal mine dust was not exclusively related to the presence of silica but resulted from a complex interaction between the different components. In silicosis and CWP, bronchoalveolar lavage showed a large influx of mononuclear phagocytes, with an increased spontaneous production of oxidants, fibronectin, neutrophil chemotactic factor, and also of interleukin-6 and TNF-alpha. This spontaneous cytokine release was associated with an increased cytokine messenger ribonucleic acid (mRNA) expression in the lungs of coal miners.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…In addition to TNF-· and IL-1, which are well-known macrophagederived growth factors [40], particulate-exposed AM also release platelet-derived growth factor (PDGF) [41] and fibroblast growth factor (FGF) [42], secretory products that cause enhanced proliferation of fibroblasts. Fibronectin, another growth-regulating protein, has also been shown to be produced by AM upon exposure to asbestos, quartz, and coal mine dusts [43].…”

Section: Release Of Cytokines and Eicosanoidsmentioning

confidence: 99%