REFRACTORY CERAMIC FIBERS ACTIVATE ALVEOLAR MACROPHAGE EICOSANOID ANDCYTOKINE RELEASE

Citation
Gd. Leikauf et al., REFRACTORY CERAMIC FIBERS ACTIVATE ALVEOLAR MACROPHAGE EICOSANOID ANDCYTOKINE RELEASE, Journal of applied physiology, 78(1), 1995, pp. 164-171
Citations number
37
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
78
Issue
1
Year of publication
1995
Pages
164 - 171
Database
ISI
SICI code
8750-7587(1995)78:1<164:RCFAAM>2.0.ZU;2-I
Abstract
Refractory ceramic fiber has been developed for industrial processes r equiring materials with high thermal and mechanical stability. To eval uate the biological activity of this fiber, rat alveolar macrophages w ere exposed for less than or equal to 24 h to 0-1,000 mu g/ml of refra ctory ceramic fiber, crocidolite asbestos, silica (fibrogenic particle s), or titanium dioxide (a nonfibrogenic particle), and eicosanoid, tu mor necrosis factor-alpha (TNF), and lactate dehydrogenase release wer e measured. Particle dimensions were determined by electron microscopy . Radioactivity coeluting with leukotriene B-4 (LTB(4)) and immunoreac tive LTB(4) and TNF release increased after refractory ceramic fiber a nd were similar in magnitude after asbestos but less than after silica . For example, the total [H-3]eicosanoid release increased 3.9-fold af ter refractory ceramic fiber, 4.6-fold after asbestos, and 8.7-fold af ter silica. Refractory ceramic fiber and asbestos also have similar pa rticle dimensions (diameter, length, and surface area). Inasmuch as ma crophage-derived LTB(4) and TNF are potent mediators in inflammatory e vents, including migration and activation of neutrophils, these findin gs suggest that refractory ceramic fiber can activate macrophages in v itro to release mediators relevant to in vivo findings of inflammation and fibrotic lung disease in laboratory animals.