Asbestosis is a fibrotic and inflammatory interstitial lung disease occurring after chronic occupational exposure to asbestos.
An alveolitis has been described with activated alveolar macrophages and increased neutrophils as sampled by bronchoalveolar lavage (BAL).
Animal models and in vitro studies demonstrate that asbestos can stimulate alveolar macrophages to release neutrophil chemotactic factor.
We performed BAL on 18 nonsmoking individuals with asbestos exposure and observed a twofold increase in percent neutrophils recovered.
Alveolar macrophages cultured in vitro from the asbestos-exposed individuals spontaneously released significant amounts of the neutrophil chemotaxin, interleukin-8 (IL-8).
In addition, the alveolar macrophages expressed a 2.7-fold increase in steady state mRNA levels compared to unexposed normal controls utilizing the reverse transcriptase/polymerase chain reaction.
In vitro experiments confirmed that crocidolite or chrysotile asbestos could stimulate the release of IL-8 from mononuclear phagocytes in a dose-dependent fashion.
We conclude that asbestos exposure causes a mild neutrophilic alveolitis, and that IL-8 is one potential mediator capable of contributing to this inflammation in the lower respiratory tract.
Mots-clés Pascal : Amiante, Exposition professionnelle, Asbestose, Homme, Alvéole pulmonaire, Neutrophile, Macrophage, Interleukine 8, Cytokine, Lavage bronchoalvéolaire, Médecine travail, Appareil respiratoire pathologie, Pneumoconiose, Maladie professionnelle, Poumon pathologie
Mots-clés Pascal anglais : Asbestos, Occupational exposure, Asbestosis, Human, Pulmonary alveolus, Neutrophil, Macrophage, Interleukin 8, Cytokine, Bronchoalveolar lavage, Occupational medicine, Respiratory disease, Pneumoconiosis, Occupational disease, Lung disease
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Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 96-0097687
Code Inist : 002B03L06. Création : 199608.