Cytokine and free radical responses of alveolar macrophages in vitro to asbestos fibres

Our plain-English summary of Cytokine and free radical responses of alveolar macrophages in vitro to asbestos fibres, by L.C. Mongan, T. Jones, G. Patrick (Cytokine, 2000).

The study

• Authors: L.C. Mongan, T. Jones, G. Patrick
• Journal: Cytokine
• Published: 2000;12(8):1243-7
• Cited by: 21 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

A method for culturing primary rat alveolar macrophages (AMs) for 14 days was used to compare their responses to crocidolite and chrysotile asbestos fibres. Exposure to crocidolite increased production of tumour necrosis factor-alpha (TNF-alpha) and interleukin 1beta (IL-1beta), whereas exposure to chrysotile did not; neither fibre altered the production of interleukin 6 (IL-6). IL-1beta production increased progressively, while TNF-alpha was fully elevated from day 1. Conversely, chrysotile, but not crocidolite, increased production of superoxide anion and nitric oxide (NO) radicals. These differential responses were only observed by extending the culture beyond the usual 1-3 days.

Copyright 2000 Academic Press.

In plain English

This laboratory report studied alveolar macrophages (lung immune cells) from adult male F-344 rats, kept in culture for 14 days rather than the usual 1 to 3 days. The cells were exposed to UICC crocidolite or chrysotile B asbestos at two main doses; crocidolite was also tested at a third, higher dose. Neither fiber significantly changed survival, defined as the percentage of macrophages remaining regardless of their functional state. Chrysotile reduced cell viability and the cells' uptake of test particles more than crocidolite did. At the higher dose, crocidolite increased production of the inflammatory signals TNF-alpha and IL-1beta. Chrysotile did not significantly change either, and neither fiber significantly changed IL-6. Conversely, the higher dose of chrysotile, but not crocidolite, significantly increased superoxide anion (from day 9) and nitric oxide (from day 4). That extra crocidolite dose, described as giving a similar fiber number, also did not produce these responses. The authors concluded that only crocidolite raised TNF-alpha and IL-1beta and only chrysotile raised free radicals. They added that the crocidolite result corresponds to the two fibers' relative carcinogenicity.

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 primary rat cells (short communication)
• Who was studied: Alveolar macrophages obtained by lung lavage from adult male F-344 rats, pooled from batches of three rats. Cytokine data were means of three experiments; free radical data were means of two experiments.
• Exposure: UICC crocidolite or chrysotile B, autoclaved, added to cultures for up to 14 days. The two main doses were printed as 5 and 25 g/ml. Crocidolite was also tested at 40 g/ml, which the authors describe as giving a similar fiber number to 25 g/ml chrysotile. Polystyrene microspheres were used as a comparison.
• Main results:
  • Neither fiber affected macrophage survival at either 5 or 25 g/ml (P>0.05). Survival was defined as the percentage of macrophages remaining, regardless of their functional state.
  • Chrysotile at both doses significantly decreased viability (P<0.001). With crocidolite the decrease was small but statistically significant.
  • Chrysotile at both doses significantly decreased particle uptake (P<0.001). Crocidolite decreased it significantly at 25 g/ml (P<0.05) but not at 5 g/ml.
  • For TNF-alpha production, 25 g/ml crocidolite differed significantly from controls (P<0.005). The lower crocidolite dose and both chrysotile doses did not.
  • For IL-1beta production, 25 g/ml crocidolite differed significantly from controls (P<0.05).
  • With crocidolite, TNF-alpha was fully raised from day 1, while IL-1beta rose continuously up to day 14.
  • Neither fiber significantly affected IL-6 production.
  • Chrysotile at 25 g/ml, but not at 5 g/ml, significantly increased superoxide anion production. This effect was not seen until day 9.
  • From day 4, chrysotile at 25 g/ml significantly increased nitric oxide production.
  • Crocidolite at 5 or 25 g/ml did not increase superoxide anion or nitric oxide.
  • Even 40 g/ml crocidolite did not produce the responses seen with 25 g/ml chrysotile. The authors describe this crocidolite dose as giving a similar fiber number concentration.
  • The authors reported that 40 g/ml crocidolite had no greater effect on viability or particle uptake than 25 g/ml; these data were not shown.
  • Polystyrene microspheres did not significantly alter these measures. On this basis, the authors judged that the fiber effects were not simply due to particle uptake.
• The authors' conclusion: The authors concluded that only crocidolite increased TNF-alpha and IL-1beta, while only chrysotile increased free radical production. They stated that the crocidolite cytokine result corresponds to the relative carcinogenicity of the two fibers.
• Limitations the authors state:
  • Baseline cytokine production by the macrophages varied considerably, possibly because they were primary cells.
  • The fibers were mainly compared at equal mass, although fiber number can matter.

Topics

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

Medical terms in this study, explained in our Lexicon: Cytokine, Alveolar Macrophage, Crocidolite, Chrysotile, Necrosis, Superoxide.

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)
• Refractory ceramic fibers activate alveolar macrophage eicosanoid and cytokine release — G.D. Leikauf, S.P. Fink, et al. (1995)
• Human alveolar macrophage cytokine release in response to in vitro and in vivo asbestos exposure — R.C. Perkins, R.K. Scheule, et al. (1993)
• Distinctive profile of alveolar macrophage-derived cytokine release induced by fibrogenic and nonfibrogenic mineral dusts — I. Lemaire, S. Ouellet (1996)
• Differential responses of murine alveolar macrophages to elongate mineral particles of asbestiform and non-asbestiform varieties: Cytotoxicity, cytokine secretion and transcriptional changes — T.O. Khaliullin, E.R. Kisin, et al. (2020)
• Glutathione release by pulmonary alveolar macrophages in response to particles in vitro — D.S. Boehme, K.R. Maples, et al. (1992)

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