Immune adherence reactivity of rat alveolar macrophages following inhalation of crocidolite asbestos

Our plain-English summary of Immune adherence reactivity of rat alveolar macrophages following inhalation of crocidolite asbestos, by K. Miller, E. Kagan (Clinical and Experimental Immunology, 1977).

The study

• Authors: K. Miller, E. Kagan
• Journal: Clinical and Experimental Immunology
• Published: 1977;29(1):152-8
• Cited by: 22 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

The immune adherence phenomenon was used to demonstrate the in vivo deposition of complement on membranes of alveolar macrophages from rats chronically exposed to crocidolite asbestos dust. Pre-treatment of macrophage cualtures with anti-C3 antiserum greatly diminished the level of immune adherence reactivity. Alveolar macrophages exposed to crocidolite asbestos in vitro did not exhibit significant levels of immune adherence reactivity. These results may reflect an in-vivo antigen-antibody-complement interaction on the surface of a alveolar macrophages from animals which have inhaled asbestos dust.

In plain English

This animal experiment, from the National Research Institute for Occupational Diseases in Johannesburg, South Africa, examined lung immune cells (alveolar macrophages) from rats that breathed crocidolite asbestos dust for 6 months, compared with unexposed rats. The authors used the immune adherence test, in which human red blood cells stick to cells carrying complement, a part of the immune system. In exposed rats, red cells stuck to 27 to 52% of macrophages (mean 34%). In unexposed rats the mean was 8%, a statistically significant difference. Sheep red cells, which cannot take part in this reaction, stuck far less to macrophages from exposed rats. Treating the cells with antiserum against the complement component C3 reduced adherence to 4 to 17%. When macrophages from unexposed rats took up crocidolite in the laboratory, the increase was not statistically significant. In a test of the alternate complement pathway, crocidolite in fresh human plasma produced no conversion products of factor B or C3. The authors concluded that the results may reflect an antigen-antibody-complement reaction on macrophages in animals that had inhaled asbestos dust.

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 (rats exposed to crocidolite by inhalation compared with unexposed control rats, with laboratory tests on their lung macrophages)
• Who was studied: Outbred adult male rats (Rattus norvegicus) at the National Research Institute for Occupational Diseases, Johannesburg, South Africa. Table 1 lists 14 exposed ('dusted') and 14 unexposed ('non-dusted') rats. Alveolar macrophages were collected by washing out the lungs.
• Exposure: U.I.C.C. crocidolite asbestos dust inhaled at 1350 fibres/cm3 (fibre length 5 to 100 micrometres), 8 hours a day, 5 days a week, for 6 months, starting at 6 months of age. Macrophages from unexposed rats were also exposed to crocidolite in the laboratory.
• Main results:
  • In exposed rats, human red blood cells adhered to 27 to 52% of alveolar macrophages (mean 34%), counted in 200 cells
  • In unexposed rats, mean immune adherence reactivity was 8%. The text gives a range of 1 to 14%, but Table 1 lists a value of 15% for one unexposed rat. The difference between exposed and unexposed rats was significant (P less than 0.01).
  • With sheep red blood cells, which lack immune adherence receptors, adherence to macrophages from exposed rats was significantly lower (P less than 0.01) and similar to that seen in unexposed rats
  • Pre-treating macrophages from exposed rats with antiserum to human or rat C3 greatly reduced adherence, to a range of 4 to 17%
  • Adding purified complement components C2 and C3 to macrophages from exposed rats produced some increase in immune adherence reactivity
  • Baboon red blood cells, which also have immune adherence receptors, gave results that paralleled those with human red cells
  • When macrophages from unexposed rats took up crocidolite in the laboratory, adherence increased only insignificantly (P greater than 0.05). The authors attributed this mainly to red cells sticking to asbestos fibres protruding from the cells.
  • Adding fresh or heat-inactivated human or rat serum to the laboratory crocidolite cultures made no difference to immune adherence reactivity
  • In tests of the alternate complement pathway, crocidolite incubated in fresh human EGTA plasma produced no conversion products of factor B or C3, even at 70 mg/ml
• The authors' conclusion: The authors concluded that the results may reflect an antigen-antibody-complement interaction on the surface of alveolar macrophages from animals that had inhaled asbestos dust. In their view, the reactivity depended on the in vivo consequences of inhaling crocidolite rather than on uptake of asbestos as such, and may be a humoral immune response to altered macrophage surface antigens.

Topics

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

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

Related studies

• Manifestations of cellular immunity in the rat after prolonged asbestos inhalation. II. Alveolar macrophage-induced splenic lymphocyte proliferation — K. Miller, E. Kagan (1981)
• In vitro reactivity of alveolar macrophages and red blood cells with asbestos fibres treated with oxalic acid, sulfur dioxide and benzo-3,4-pyrene — M.C. Jaurand, L. Magne, et al. (1981)
• Phagocytosis of asbestos fibers by human pulmonary alveolar macrophages — T. McLemore, M. Corson, et al. (1979)
• Sialic acid mediates the initial binding of positively charged inorganic particles to alveolar macrophage membranes — J.E. Gallagher, G. George, et al. (1987)
• Leaching of chrysotile asbestos in human lungs. Correlation with in vitro studies using rabbit alveolar macrophages — M.C. Jaurand, J. Bignon, et al. (1977)
• Effects of asbestos on the random migration of rabbit alveolar macrophages — Q.N. Myrvik, E.A. Knox, et al. (1985)

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