Superoxide Anion Generation by Alveolar Inflammatory Cells in Simple Pneumoconiosis and in Progressive Massive Fibrosis of Nonsmoking Coal Worters

Wallaert, B.; Lassalle, Philippe; F, Fortin; Aerts, C; Bart, F.; Fournier, E; Voisin, C

doi:10.1164/ajrccm/141.1.129

Cited by 75 publications

(32 citation statements)

References 17 publications

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“…Indeed, a relationship has been reported between the level of oxidant production by pulmonary phagocytes and lung damage and severity of pneumoconiosis (84,94). Silica-and/or coal dust-induced oxidant production from alveolar macrophages has been measured directly or by monitoring chemiluminescence in cellular, animal, and human exposure studies.…”

Section: Activation Ofoxidant Species Production By Alveolar Macrophagesmentioning

confidence: 99%

Silicosis and coal workers' pneumoconiosis.

Castranova

Vallyathan

2000

Environ Health Perspect

306

179

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Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; o) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.

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Section: Activation Ofoxidant Species Production By Alveolar Macrophagesmentioning

confidence: 99%

Silicosis and coal workers' pneumoconiosis.

Castranova

Vallyathan

2000

Environ Health Perspect

306

179

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“…ROS are released from alveolar macrophages and leucocytes during the phagocytosis of inhaled dust particles. Furthermore, dust particles themselves can produce ROS [3].…”

Section: Introductionmentioning

confidence: 99%

Platelet Indices in Patients with Coal Workers’ Pneumoconiosis

Uygur

Örnek

Tanrıverdi

et al. 2016

Lung

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“…The ability of these cells to generate highly reactive oxygen species (ROS), including super-oxide anion, following activation of a membraneassociated reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important part of the host defence system, and has also been implicated in inflammation in a variety of pulmonary diseases [2,3], including asthma [4,5]. Oxygen metabolites cause tissue injury, smooth muscle contraction, increased airway vascular permeability, and may increase airway responsiveness and release of var-ious mediators [4].…”

mentioning

confidence: 99%

Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients

Majori

Vachier²,

Godard³

et al. 1998

Eur Respir J

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Bronchial asthma is a chronic inflammatory disease of the airways characterized by an increased recruitment of inflammatory cells, including mononuclear phagocytic cells such as monocytes [1]. The ability of these cells to generate highly reactive oxygen species (ROS), including super-oxide anion, following activation of a membraneassociated reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important part of the host defence system, and has also been implicated in inflammation in a variety of pulmonary diseases [2,3], including asthma [4,5]. Oxygen metabolites cause tissue injury, smooth muscle contraction, increased airway vascular permeability, and may increase airway responsiveness and release of var-ious mediators [4].In previous studies, it has been shown that alveolar macrophages [6], blood monocytes [5] and eosinophils [7] from asthmatic patients were able to produce high amounts of ROS. Alveolar macrophage activation was correlated with the severity of asthma [6]. This activation occurred immediately after antigen challenge, and the appearance of high-density macrophages which release higher amounts of superoxide anion occurred during the late airway response [8]. Several investigators have also suggested that polymorphonuclear leucocytes from asthmatic patients generated more ROS than control subjects [9,10]. This activation was correlated with the level of bronchial hyperreactivity [11].Corticosteroids are the most potent anti-inflammatory agents available for the treatment of asthma [12], but little is known about their molecular mechanism of action in improving symptoms or the way they reduce hyperresponsiveness. It has been proposed that corticosteroids inhibit the inflammatory process by redirection of lymphocyte traffic, inhibition of cytokine gene expression [13] and inhibition of the expression of adhesion molecules [14].The effect of anti-inflammatory corticosteroids on oxygen radical production by phagocytes has been less extensively studied, and the results are contradictory. In vitro studies have demonstrated an inhibitory effect of high corticosteroid concentrations on oxygen radical production in human granulocytes [15]. In contrast, dexamethasone treatment has been reported to have no effect on ROS secretion in human blood-derived macrophages [16], but have a stimulatory effect on human monocytes [17]. It has been reported that in vivo corticosterone had no effect on murine peritoneal inflammatory cells [18]. Ex vivo inhaled steroid treatment had no effect on superoxide anion production in human alveolar macrophages [19,20]. In contrast, a recent study showed that in vivo administration of dexamethasone or methylprednisolone led to a dose-dependent inhibition of rat peritoneal leucocyte chemiluminescence [21]. Moreover, hydrocortisone was found to inhibit superoxide anion production during an asthma attack [22].Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients. M. Majori, I. Vachier, P. Godard, M. Farce, J. Bousquet, P. Chanez. ...

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Superoxide Anion Generation by Alveolar Inflammatory Cells in Simple Pneumoconiosis and in Progressive Massive Fibrosis of Nonsmoking Coal Worters

Cited by 75 publications

References 17 publications

Silicosis and coal workers' pneumoconiosis.

Silicosis and coal workers' pneumoconiosis.

Platelet Indices in Patients with Coal Workers’ Pneumoconiosis

Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients

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