Interleukin 1 production and accessory cell function of rat alveolar macrophages exposed to mineral dust particles

Our plain-English summary of Interleukin 1 production and accessory cell function of rat alveolar macrophages exposed to mineral dust particles, by Y. Oghiso, Y. Kubota (Microbiology and Immunology, 1987).

The study

• Authors: Y. Oghiso, Y. Kubota
• Journal: Microbiology and Immunology
• Published: 1987;31(3):275-87
• Cited by: 27 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Immunostimulatory effects of respirable mineral dust particles on alveolar macrophages (AM) and T lymphocytes were tested in vitro. When rat AM were incubated with fibrogenic silica and asbestos particles, a significant interleukin 1 (IL-1) activity was generated into the culture supernatants, whereas neither AM alone nor AM incubated with non-fibrogenic titanium dioxide (TiO2) particles, however, produced a detectable amount of IL-1. Interleukin 2 (IL-2) activity, as tested with IL-2-dependent CTLL-2 assays, was not detectable from all of these cultures. It was also revealed that concanavalin A-induced proliferation of T lymphocytes was enhanced in autologous AM and nylon wool-passed spleen cell co-cultures incubated only with fibrogenic particles, but not with non-fibrogenic particles. Higher IL-1 activity was detected only from co-cultures exposed to fibrogenic particles, whereas IL-2 activity was almost similar among these co-cultures. These results indicate the differences in immunostimulatory effects on pulmonary macrophages and T lymphocytes among a variety of mineral dust particles.

In plain English

In this laboratory study of cells, the authors took alveolar macrophages (immune cells from the lung's air sacs) from male Wistar rats and exposed them in culture to three kinds of silica, to crocidolite asbestos, or to titanium dioxide, which the authors describe as non-fibrogenic. They measured interleukin 1 (IL-1) and interleukin 2 (IL-2), signaling substances of the immune system. After 48 hours, IL-1 activity was detected in fluid from macrophages exposed to the silicas or crocidolite, but not from unexposed macrophages or those exposed to titanium dioxide. IL-2 was not detected from any of the macrophage cultures. The macrophages were also grown with T lymphocytes from the same rats' spleens, together with a stimulant. In these mixed cultures, silica and crocidolite enhanced T cell growth, while unexposed and titanium dioxide-exposed macrophages only suppressed it. IL-2 levels did not differ significantly among these mixed cultures. The authors concluded that IL-1 production by these macrophages can be potentiated only by fibrogenic dusts and not by titanium dioxide. They suggested this may be relevant to how mineral dusts cause lung fibrosis.

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 using rat cells
• Who was studied: Alveolar macrophages and spleen T lymphocytes from male inbred Wistar (W/M) rats weighing 300-350 g, at the National Institute of Radiological Sciences, Chiba, Japan. Thymocytes from C3H/HeJ mice were used to test for IL-1. The number of rats is not stated.
• Exposure: In culture, cells were exposed to silica (a Sigma mixture of microcrystalline and amorphous particles), alpha-quartz silica, Min-u-sil microcrystalline silica, crocidolite asbestos (UICC standard reference preparation) or titanium dioxide, at 10-250 micrograms per milliliter
• Main results:
  • At 48 hours, IL-1 activity was detected in supernatants from macrophage cultures containing any of the three silicas or crocidolite asbestos. Control cultures without particles showed no detectable IL-1.
  • Macrophage cultures exposed to titanium dioxide showed no significant IL-1 activity.
  • IL-2 activity was not detected from any of the macrophage cultures.
  • Adding indomethacin or catalase made no significant difference to IL-1 activity in the silica- or asbestos-exposed macrophage cultures.
  • In co-cultures with T lymphocytes, silica- and alpha-quartz-exposed macrophages enhanced T cell proliferation when small numbers of macrophages were added (1.2-5.0% of the spleen cells).
  • Min-u-sil silica and crocidolite asbestos enhanced T cell responses more effectively. Titanium dioxide-exposed macrophages, like control macrophages, were only suppressive.
  • The optimal concentration of silica or asbestos for supporting T cell responses was 100-250 micrograms per milliliter. Titanium dioxide did not enhance responses at any concentration.
  • Catalase inhibited the suppression of T cell growth seen with large numbers of macrophages. Indomethacin had little effect.
  • In co-cultures, IL-1 activity rose with macrophage numbers in silica- or asbestos-exposed cultures. No IL-1 was detected in control or titanium dioxide co-cultures.
  • IL-2 levels in co-cultures increased slightly but did not differ significantly between control and dust-exposed co-cultures.
  • The proportion of macrophages carrying Ia antigen did not differ significantly among the dust-exposed co-cultures.
• The authors' conclusion: The authors concluded that IL-1 production by alveolar macrophages can be potentiated only by fibrogenic dust particles (silica and asbestos), not by non-fibrogenic titanium dioxide. They suggested that the different effects of dust-exposed macrophages may be relevant to how respirable mineral dusts cause pulmonary fibrosis.

Topics

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Fibrogenic, Macrophage.

Related studies

• Heterogeneity in immunologic functions of rat alveolar macrophages--their accessory cell function and IL-1 production — Y. Oghiso (1987)
• Secretion of fibronectin by mineral dust-derived alveolar macrophages and activated peritoneal macrophages — R. Davies, G. Erdogdu (1989)
• Polyvinylpyridine-N-oxide and carboxymethyl cellulose inhibit mineral dust-induced production of reactive oxygen species by human macrophages — P. Nyberg (1991)
• Response of bovine alveolar macrophages in vitro to welding fume particles — L.R. White, A.B. Marthinsen, et al. (1983)
• Stimulation of oxidant production in alveolar macrophages by pollutant and latex particles — G.E. Hatch, D.E. Gardner, et al. (1980)
• Enhanced interleukin activity following asbestos inhalation — D.P. Hartmann, M.M. Georgian, et al. (1984)

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