Chronic beryllium disease, which results from occupational exposure to particulate beryllium, is characterized by the development of lung granulomas and progressive pulmonary fibrosis.
Increased production of proinflammatory cytokines (e.g., tumor necrosis factor alpha and interleukin-1 beta) by pulmonary alveolar macrophages occurs in many chronic fibrotic lung diseases and is thought to contribute to the disease process.
The purpose of the present study was to investigate cytokine production by human monocytic cells exposed to beryllium in vitro.
The results indicated that such cells respond to beryllium ions in the presence of fluoride by accumulation of messenger ribonucleic acid for both tumor necrosis factor alpha and interleukin-1 beta.
These findings suggest that inhaled beryllium may directly stimulate the production of these cytokines by alveolar macrophages in vivo.
Mots-clés Pascal : Béryllium, Toxicité, Exposition professionnelle, Médecine travail, Expression génique, Facteur nécrose tumorale alpha, Homme, Fibrose, Poumon, Pneumopathie interstitielle, Mécanisme action, Cytokine, Interleukine 1bêta, Inhalation, Appareil respiratoire pathologie, In vitro, Macrophage, Alvéole pulmonaire, Lignée THP1
Mots-clés Pascal anglais : Beryllium, Toxicity, Occupational exposure, Occupational medicine, Gene expression, Tumor necrosis factor alpha, Human, Fibrosis, Lung, Interstitial pneumonitis, Mechanism of action, Cytokine, Interleukin 1bêta, Inhalation, Respiratory disease, In vitro, Macrophage, Pulmonary alveolus
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 96-0224171
Code Inist : 002B03L05. Création : 199608.