Refractory ceramic fibers activate alveolar macrophage eicosanoid and cytokine release

Our plain-English summary of Refractory ceramic fibers activate alveolar macrophage eicosanoid and cytokine release, by G.D. Leikauf, S.P. Fink, M.L. Miller, et al (Journal of Applied Physiology, 1995).

The study

• Authors: G.D. Leikauf, S.P. Fink, M.L. Miller, J.E. Lockey, K.E. Driscoll
• Journal: Journal of Applied Physiology
• Published: 1995;78(1):164-71
• Cited by: 21 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Refractory ceramic fiber has been developed for industrial processes requiring materials with high thermal and mechanical stability. To evaluate the biological activity of this fiber, rat alveolar macrophages were exposed for < or = 24 h to 0-1,000 micrograms/ml of refractory ceramic fiber, crocidolite asbestos, silica (fibrogenic particles), or titanium dioxide (a nonfibrogenic particle), and eicosanoid, tumor necrosis factor-alpha (TNF), and lactate dehydrogenase release were measured. Particle dimensions were determined by electron microscopy. Radioactivity coeluting with leukotriene B4 (LTB4) and immunoreactive LTB4 and TNF release increased after refractory ceramic fiber and were similar in magnitude after asbestos but less than after silica. For example, the total [3H]eicosanoid release increased 3.9-fold after refractory ceramic fiber, 4.6-fold after asbestos, and 8.7-fold after silica. Refractory ceramic fiber and asbestos also have similar particle dimensions (diameter, length, and surface area). Inasmuch as macrophage-derived LTB4 and TNF are potent mediators in inflammatory events, including migration and activation of neutrophils, these findings suggest that refractory ceramic fiber can activate macrophages in vitro to release mediators relevant to in vivo findings of inflammation and fibrotic lung disease in laboratory animals.

In plain English

This was a cell-culture study. The authors exposed alveolar macrophages (lung immune cells) from male Fischer 344 rats to refractory ceramic fiber, crocidolite asbestos, silica or titanium dioxide at 10 to 1,000 micrograms per milliliter for up to 24 hours. They measured release of inflammatory signaling substances, including leukotriene B4 and tumor necrosis factor, and of an enzyme that marks cell damage. At 1,000 micrograms per milliliter, total labeled eicosanoid release rose 3.9-fold with ceramic fiber, 4.6-fold with asbestos and 8.7-fold with silica. Release with titanium dioxide did not differ significantly from untreated cells. After 24 hours, ceramic fiber significantly increased leukotriene B4 at 300 and 1,000 micrograms per milliliter; at 30 and 100, levels were not significantly different from untreated cells. Its leukotriene B4 and tumor necrosis factor responses were smaller than those to the same dose of asbestos. It increased cell damage modestly, much less than silica did. The authors concluded that the fiber can activate macrophages in vitro to release mediators relevant to inflammation and fibrotic lung disease in laboratory animals. They noted that particle size, shape, density and surface area were not standardized.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: In vitro laboratory experiment on rat lung cells (alveolar macrophages) in culture, comparing refractory ceramic fiber with crocidolite asbestos, silica and titanium dioxide
• Who was studied: Alveolar macrophages obtained by lung lavage from male pathogen-free Fischer 344 rats (250-300 g); the number of rats is not stated
• Exposure: Cells were exposed for up to 24 hours to 10 to 1,000 micrograms per milliliter of refractory ceramic fiber, crocidolite asbestos, alpha-quartz silica, titanium dioxide (described as a nuisance dust), or no particles (control). The ceramic fiber was a mixture of alumina (49%) and silica (50%).
• Main results:
  • Total labeled eicosanoid release increased 3.9-fold after refractory ceramic fiber, 4.6-fold after asbestos and 8.7-fold after silica
  • After 24 hours, release with 1,000 micrograms per milliliter of refractory ceramic fiber was 18.3 plus or minus 1.7 times 10 to the 4th dpm per well, compared with 4.7 plus or minus 0.3 times 10 to the 4th in controls (P less than 0.05)
  • At the same dose, release with silica was 41.1 plus or minus 3.5 and with asbestos 21.6 plus or minus 2.2 times 10 to the 4th dpm per well
  • Refractory ceramic fiber at 300 micrograms per milliliter also significantly increased released radioactivity (11.5 plus or minus 1.1 times 10 to the 4th dpm per well); at 10, 30 and 100 micrograms per milliliter the increase was not statistically significant
  • Radioactivity released from macrophages treated with titanium dioxide (10 to 1,000 micrograms per milliliter) was not significantly different from medium alone
  • By immunoassay, eicosanoid levels after 30 or 100 micrograms per milliliter of refractory ceramic fiber were not significantly different from control
  • Refractory ceramic fiber at 300 and 1,000 micrograms per milliliter, and asbestos at 1,000, increased leukotriene B4 and prostaglandin E2 release after 24 hours
  • At an equal dose (1,000 micrograms per milliliter), the eicosanoid response to refractory ceramic fiber was less than that to asbestos
  • Tumor necrosis factor release was increased by both refractory ceramic fiber and asbestos; the response to refractory ceramic fiber was less than to an equal dose of asbestos
  • Chromatography showed that leukotriene B4 release increased after refractory ceramic fiber or asbestos
  • Cell damage (lactate dehydrogenase release) after 100, 300 or 1,000 micrograms per milliliter of refractory ceramic fiber rose modestly, to 158 plus or minus 21, 174 plus or minus 10 and 295 plus or minus 13% of control
  • Silica at 1,000 micrograms per milliliter raised lactate dehydrogenase release to 896% of control (72.2% of total cellular activity)
  • The median length of the refractory ceramic fiber was about twice that of the asbestos
• The authors' conclusion: The authors concluded that refractory ceramic fiber can activate macrophages in vitro to release mediators relevant to the inflammation and fibrotic lung disease seen in laboratory animals
• Limitations the authors state:
  • Particle size, shape, density and surface area are likely to affect dose-response comparisons, and these variables were not standardized in the tests
  • The authors cautioned against placing too much emphasis on in vitro cytotoxicity tests when interpreting in vivo significance
  • Cell damage (lactate dehydrogenase release) was not measured after asbestos exposure in this study

Topics

The National Library of Medicine indexes this study under subjects our site covers: Crocidolite.

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Cytokine, Crocidolite, Fibrogenic, Tumor Necrosis Factor-alpha (TNF-α), Lactate Dehydrogenase (LDH), Macrophage, Inflammation.

Related studies

• Alveolar macrophage cytokine and growth factor production in a rat model of crocidolite-induced pulmonary inflammation and fibrosis — K.E. Driscoll, J.K. Maurer, et al. (1995)
• Mechanism of refractory ceramic fiber- and rock wool-induced cytotoxicity in alveolar macrophages — K.A. Kim, W.K. Lee, et al. (2001)
• Distinctive profile of alveolar macrophage-derived cytokine release induced by fibrogenic and nonfibrogenic mineral dusts — I. Lemaire, S. Ouellet (1996)
• Cytokine and free radical responses of alveolar macrophages in vitro to asbestos fibres — L.C. Mongan, T. Jones, et al. (2000)
• Human alveolar macrophage cytokine release in response to in vitro and in vivo asbestos exposure — R.C. Perkins, R.K. Scheule, et al. (1993)
• Asbestos stimulation triggers differential cytokine release from human monocytes and alveolar macrophages — L.J. Geist, L.S. Powers, et al. (2000)

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