Effects of asbestos fibers on alveolar macrophage-mediated lymphocyte cytostasis

Our plain-English summary of Effects of asbestos fibers on alveolar macrophage-mediated lymphocyte cytostasis, by B.E. Bozelka, P. Sestini, Y. Hammad, et al (Environmental Research, 1986).

The study

• Authors: B.E. Bozelka, P. Sestini, Y. Hammad, J.E. Salvaggio
• Journal: Environmental Research
• Published: 1986;40(1):172-80
• Cited by: 1 article, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Prolonged asbestos inhalation results in pulmonary inflammation and fibrosis. Since alveolar macrophages are active in regulation of immune responses in lung and appear to be involved in the pathogenesis of asbestosis, we evaluated the effects of asbestos exposure on the ability of these cells to regulate lymphocyte function. Alveolar macrophages obtained by lung lavage from BALB/C mice were treated in vitro with either UICC amosite or chrysotile asbestos and the effects on lymphocyte cytostasis compared with those of macrophages incubated with latex beads or zymosan. Macrophages (10%) incubated either alone or with latex beads for 48 hr effectively inhibited lymphocyte mitogenesis. However, alveolar macrophages incubated with either amosite or chrysotile asbestos did not demonstrate intact cytostatic activity. Decreased viability of chrysotile asbestos-treated macrophages correlated with loss of cytostatic effects, but alveolar macrophages exposed to amosite remained viable. We conclude, therefore, that exposure of alveolar macrophages to asbestos can result in loss of their ability to down-regulate lymphocyte proliferation, a finding which may be important in the pathogenesis of asbestos-related disease.

In plain English

This was a laboratory study of mouse cells, not of people. The authors washed alveolar macrophages (immune cells that clear dust from the lungs) out of the lungs of female BALB/C mice. In culture, they tested whether these cells could still hold back the multiplication of stimulated spleen lymphocytes after contact with UICC chrysotile or amosite asbestos, latex beads, or zymosan particles. Macrophages kept 48 hours in plain medium or with latex beads still suppressed lymphocyte growth. After 48 hours with either asbestos fiber, that ability was largely lost, although macrophages given a lower, nontoxic chrysotile dose kept it. Chrysotile reduced macrophage viability (50% at 48 hours, and as low as 6% after 96 hours at the highest dose). Amosite-treated macrophages stayed about as viable as controls. The chrysotile effect appeared after as little as 1 hour. Zymosan also reduced suppression, and macrophages from the abdominal cavity responded like lung macrophages. The authors concluded that asbestos exposure can make these cells lose their ability to restrain lymphocyte proliferation. They said the relevance to disease still has to be tested in animal models and in other species.

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 mouse cells
• Who was studied: Two- to three-month-old female BALB/C mice raised in the authors' animal facility. Alveolar macrophages were obtained by lung lavage, peritoneal macrophages from mineral-oil-injected mice, and lymphocytes from spleens. The number of mice is not stated.
• Exposure: UICC chrysotile and amosite asbestos fibers added to macrophage cultures, compared with latex beads and serum-treated zymosan. Methods give chrysotile 0.15 mg/ml and amosite 0.11 mg/ml; tables give doses per well (for example amosite 2.2 and 4.4 micrograms per well, chrysotile 0.3 to 3.2 micrograms per well).
• Main results:
  • Alveolar macrophages preincubated 48 hours in medium alone still inhibited lymphocyte blastogenesis.
  • Alveolar macrophages preincubated 48 hours with amosite (2.2 micrograms per well) or chrysotile (3 micrograms per well in Table 1; 1.6 micrograms per well in Table 2) largely lost their ability to suppress lymphocyte proliferation.
  • Chrysotile-treated macrophages had reduced viability (50%). In the same experiment, viability was 83% for control and 88% for amosite-treated macrophages.
  • Over 24 and 96 hours, amosite (2.2 and 4.4 micrograms per well) did not significantly change macrophage viability (91 to 94%, versus control 96% and 94%). Chrysotile at 0.8, 1.6 and 3.2 micrograms per well reduced viability to 61%, 48% and 35% at 24 hours and to 24%, 11% and 6% at 96 hours.
  • When untreated preincubated macrophages were added to lymphocyte cultures containing chrysotile, suppression was significantly reduced (70,507 counts per minute) compared with amosite-containing or control cultures. With amosite, suppression was complete.
  • Latex beads did not affect macrophage suppressive activity. Serum-activated zymosan significantly reduced it without affecting viability.
  • Macrophages given a nontoxic concentration of chrysotile (0.3 micrograms per well in Table 2, viability 85%) kept their suppressive activity.
  • The suppressive activity of chrysotile-treated macrophages was diminished after 1 hour and fell progressively from 4 through 24 hours. Amosite showed a similar but less pronounced pattern.
  • Peritoneal macrophages also suppressed lymphocyte mitogenesis. Exposure to amosite or chrysotile for 48 hours significantly reduced this ability, as with alveolar macrophages.
  • Fibers added directly to lymphocytes did not significantly change responses at optimal or suboptimal Con A doses. Both fibers significantly enhanced responses at a supraoptimal Con A dose.
• The authors' conclusion: The authors concluded that both chrysotile and amosite could significantly suppress macrophage-mediated regulation of lymphocytes. They suggested this loss of control might account for some immunologic abnormalities seen in patients with asbestosis, such as hypergammaglobulinemia and autoantibody formation.
• Limitations the authors state:
  • The relevance of these in vitro findings to disease has to be established in animal model studies.
  • Macrophage effects on lymphocytes differ among animal species, so the results need confirmation using macrophages from other experimental animals.

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, Inflammation, Fibrosis, Asbestos Exposure, UICC, Amosite, Chrysotile, 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)
• Response of perifused alveolar macrophages to glass fibers: effect of exposure duration and fiber length — G. Forget, M.J. Lacroix, et al. (1986)
• Phagocytosis of asbestos fibers by human pulmonary alveolar macrophages — T. McLemore, M. Corson, et al. (1979)
• Asbestos fibers and silica particles stimulate rat alveolar macrophages to release tumor necrosis factor. Autoregulatory role of leukotriene B4 — C.M. Dubois, E. Bissonnette, et al. (1989)
• Comparison of phagocytosis of uncoated versus coated asbestos fibers by cultured human pulmonary alveolar macrophages — T.L. McLemore, V. Roggli, et al. (1981)
• Effects of asbestos on the random migration of rabbit alveolar macrophages — Q.N. Myrvik, E.A. Knox, et al. (1985)

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