Secretion of fibronectin by mineral dust-derived alveolar macrophages and activated peritoneal macrophages

Our plain-English summary of Secretion of fibronectin by mineral dust-derived alveolar macrophages and activated peritoneal macrophages, by R. Davies, G. Erdogdu (Experimental Lung Research, 1989).

The study

• Authors: R. Davies, G. Erdogdu
• Journal: Experimental Lung Research
• Published: 1989;15(2):285-97
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The in vitro secretion of fibronectin by rat alveolar macrophages recovered following the intratracheal instillation of various mineral dusts was examined using a competitive enzyme-linked immunoassay (CELIA) method. Cells derived with the fibrogenic dusts DQ12 quartz and UICC crocidolite asbestos had elevated rates of fibronectin secretion when compared ith those derived from titanium dioxide or saline. The in vitro culture of alveolar macrophages with dusts did not lead to elevated rates of fibronectin secretion, suggesting that mechanisms other than the direct interaction between dusts and macrophages may be responsible for elevated rates of fibronectin secretion by cells exposed to fibrogenic dusts. This suggests that fibronectin deposition seen in pneumoconiotic lesions in immunohistochemical studies may in part have been derived from macrophages. Thioglycollate-induced activated mouse peritoneal macrophages secreted significantly less fibronectin than resident peritoneal macrophages, a finding contrasting with those of Tsukamoto et al. [7].

In plain English

The authors put quartz (25 mg), UICC crocidolite asbestos (10 mg), titanium dioxide (25 mg) or saline into female Fischer rats' windpipes. They then measured fibronectin, a protein, released in culture by scavenger cells (alveolar macrophages) washed from the lungs. At 2 to 3 months, cells from quartz-treated lungs released significantly more than cells from crocidolite-treated lungs, which released more than titanium dioxide or saline cells. For cells collected after 2 weeks, release in the first 24 hours of culture, in nanograms per microgram of cell DNA, was 68 plus or minus 10 (crocidolite), 53 plus or minus 5 (quartz), 21 plus or minus 4 (titanium dioxide) and 13 plus or minus 1 (saline). Dusts added directly to cultured macrophages from untreated rats lowered fibronectin release. In mice, resident abdominal macrophages released significantly more fibronectin than thioglycollate-activated ones. The authors concluded macrophages may contribute to fibronectin in dust-induced fibrotic lesions; they saw no direct dust stimulation in culture but said it might occur in living lungs. In the main experiment, each treatment's cells came from one rat, which the authors called typical of four per group.

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: Animal experiment with cell culture: dust instillation in living rats followed by culture of macrophages washed from the lungs; dusts added directly to cultured macrophages; comparison of mouse peritoneal macrophages
• Who was studied: Twelve-week-old female specific-pathogen-free Fischer (F344) rats. In the main time-course experiment, the cells for each treatment came from one animal; the authors described the results as typical of each group of four treated animals. Female Swiss TO mice supplied the peritoneal macrophages.
• Exposure: Intratracheal instillation of DQ12 quartz (25 mg), UICC crocidolite asbestos (10 mg), titanium dioxide (25 mg) or saline. Separately, dusts were added directly to cultured alveolar macrophages from nondusted rats. Mice received intraperitoneal thioglycollate broth, saline, or no treatment.
• Main results:
  • In rats lavaged 2 to 3 months after instillation, macrophages from quartz-instilled lungs secreted significantly more fibronectin than those from crocidolite-treated lungs. Crocidolite-derived cells in turn secreted more than cells from titanium dioxide- or saline-instilled lungs.
  • In cells obtained 2 weeks after instillation, fibronectin secretion rates for the first 24 hours in culture, in nanograms per microgram of DNA, were: saline 13 plus or minus 1; titanium dioxide 21 plus or minus 4; quartz 53 plus or minus 5; crocidolite 68 plus or minus 10. The authors described secretion after the fibrogenic dusts as significantly elevated compared with saline or an inert dust.
  • When cells were cultured in fibronectin-depleted newborn calf serum instead, secretion was considerably elevated in all populations. In that experiment, crocidolite-derived cells secreted at a rate similar to titanium dioxide or saline cells; the authors said this was a feature of cells from animals lavaged 4 to 6 months after instillation.
  • The article reports that even after 3 months there was no evidence of lung fibrosis after crocidolite treatment, whereas extensive fibrosis always follows quartz treatment. This is attributed to a personal communication.
  • When dusts were added directly to cultured alveolar macrophages from nondusted rats, fibronectin secretion over 24 hours was significantly decreased rather than enhanced, especially at the higher dust amount (mean plus or minus SE, n = 3). No dust gave 530 plus or minus 76. Titanium dioxide gave 436 plus or minus 22 at the lower amount and 288 plus or minus 82 at the higher. Quartz gave 317 plus or minus 18 and 130 plus or minus 68. Crocidolite gave 418 plus or minus 22 and 182 plus or minus 19. The authors suggested quartz and crocidolite were likely cytotoxic at the high concentrations.
  • Resident mouse peritoneal macrophages secreted significantly more fibronectin in culture than thioglycollate-elicited activated cells. Cells from saline-injected mice gave the same result as cells from noninjected mice.
• The authors' conclusion: The authors concluded that alveolar macrophages recovered after instillation of fibrogenic dusts have elevated fibronectin secretion, so macrophages may contribute to fibronectin deposition in fibrotic lesions. They wrote that the dusts appeared unable to stimulate secretion by direct interaction with macrophages in their experiments. They also allowed that adhesion to plastic might have masked a direct effect, and that direct stimulation might occur in the living lung.
• Limitations the authors state:
  • For each dust or saline treatment in the time-course experiment, the macrophages came from one animal, because no more than four rats could be studied on a single day.
  • The macrophages were already adhering to plastic dishes, which may have masked any direct effect of the particles.
  • Dusts might stimulate secretion in the living lung through interactions with lung components that could not be simulated in culture.
  • Some of the fibronectin measured in culture may have come off the surfaces of the macrophages rather than being newly secreted.
  • The authors had no explanation for why the type of calf serum changed fibronectin secretion.
  • The contrast with Tsukamoto et al. may reflect a species difference (guinea pigs versus mice) or different fibronectin detection methods.

Topics

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

Related studies

• Stimulation of alveolar macrophages by mineral dusts in vitro: luminol-dependent chemiluminescence study — V. Vilím, J. Wilhelm, et al. (1987)
• Activated alveolar macrophages express the insulin-like growth factor-I receptor — W.N. Rom, P. Pääkkö (1991)
• Interleukin 1 production and accessory cell function of rat alveolar macrophages exposed to mineral dust particles — Y. Oghiso, Y. Kubota (1987)
• Cytotoxic effects of some mineral dusts on Syrian hamster peritoneal macrophages — E. Bey, J.S. Harington (1971)
• Inorganic particles induce secretion of a macrophage homologue of platelet-derived growth factor in a density-and time-dependent manner in vitro — R.M. Schapira, A.R. Osornio-Vargas, et al. (1991)
• Polyvinylpyridine-N-oxide and carboxymethyl cellulose inhibit mineral dust-induced production of reactive oxygen species by human macrophages — P. Nyberg (1991)

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