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Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.

Rats were exposed by inhalation to coal mine dust, titanium dioxide, or quartz. The magnitude of the consequent inflammatory response was assessed by counting numbers and types of leukocytes in the bronchoalveolar lavage fluid. The magnitude of the inflammatory response reflected the toxicity of the...

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Detalles Bibliográficos
Autores principales: Brown, G M, Brown, D M, Donaldson, K
Formato: Texto
Lenguaje:English
Publicado: 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1519538/
https://www.ncbi.nlm.nih.gov/pubmed/1396472
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author Brown, G M
Brown, D M
Donaldson, K
author_facet Brown, G M
Brown, D M
Donaldson, K
author_sort Brown, G M
collection PubMed
description Rats were exposed by inhalation to coal mine dust, titanium dioxide, or quartz. The magnitude of the consequent inflammatory response was assessed by counting numbers and types of leukocytes in the bronchoalveolar lavage fluid. The magnitude of the inflammatory response reflected the toxicity of the dusts, with quartz eliciting the greatest recruitment of inflammatory leukocytes, coal mine dust less than quartz, and titanium dioxide eliciting no inflammation. To assess the persistence of the inflammation, groups of rats were maintained in room air for 30 or 60 days after cessation of dust exposure and then numbers of leukocytes were assessed. Bronchoalveolar leukocytes in rats exposed to coal mine dust were reduced after exposure, but in the quartz-exposed rats the numbers increased with time after exposure. The chemotactic responses of bronchoalveolar leukocytes from rats inhaling coal mine dust and quartz were reduced and remained so after a 30-day recovery period. Their reduced ability to chemotact did not fully prevent macrophages from leaving the bronchoalveolar region of dust-exposed rats. However, it is likely that the delayed removal of inflammatory leukocytes with the potential to injure the lung tissue may contribute to septal damage and so contribute to the pathogenesis of pneumoconiosis.
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spelling pubmed-15195382006-07-26 Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure. Brown, G M Brown, D M Donaldson, K Environ Health Perspect Research Article Rats were exposed by inhalation to coal mine dust, titanium dioxide, or quartz. The magnitude of the consequent inflammatory response was assessed by counting numbers and types of leukocytes in the bronchoalveolar lavage fluid. The magnitude of the inflammatory response reflected the toxicity of the dusts, with quartz eliciting the greatest recruitment of inflammatory leukocytes, coal mine dust less than quartz, and titanium dioxide eliciting no inflammation. To assess the persistence of the inflammation, groups of rats were maintained in room air for 30 or 60 days after cessation of dust exposure and then numbers of leukocytes were assessed. Bronchoalveolar leukocytes in rats exposed to coal mine dust were reduced after exposure, but in the quartz-exposed rats the numbers increased with time after exposure. The chemotactic responses of bronchoalveolar leukocytes from rats inhaling coal mine dust and quartz were reduced and remained so after a 30-day recovery period. Their reduced ability to chemotact did not fully prevent macrophages from leaving the bronchoalveolar region of dust-exposed rats. However, it is likely that the delayed removal of inflammatory leukocytes with the potential to injure the lung tissue may contribute to septal damage and so contribute to the pathogenesis of pneumoconiosis. 1992-07 /pmc/articles/PMC1519538/ /pubmed/1396472 Text en
spellingShingle Research Article
Brown, G M
Brown, D M
Donaldson, K
Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.
title Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.
title_full Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.
title_fullStr Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.
title_full_unstemmed Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.
title_short Persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.
title_sort persistent inflammation and impaired chemotaxis of alveolar macrophages on cessation of dust exposure.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1519538/
https://www.ncbi.nlm.nih.gov/pubmed/1396472
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