Differences between particulate and peptide stimuli on activation of oxidant production in alveolar macrophages

Our plain-English summary of Differences between particulate and peptide stimuli on activation of oxidant production in alveolar macrophages, by G.E. Hatch, A. Spock, D.E. Gardner, et al (Chest, 1980).

The study

• Authors: G.E. Hatch, A. Spock, D.E. Gardner, D.B. Menzel
• Journal: Chest
• Published: 1980;77(2 Suppl):267-9
• Cited by: 5 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

The authors compared the oxidant production (respiratory burst) of alveolar macrophages stimulated by particles with that stimulated by a soluble peptide. Alveolar macrophages were obtained by lung lavage from guinea pigs, rabbits, rats, mice and hamsters. Human lavage cells came from therapeutic lung lavage at Duke Medical Center of patients with cystic fibrosis and alveolar proteinosis, and from small exploratory lavage samples of patients with pneumonia, lung cancer, asthma and bronchitis. The patients were aged 8 days to 58 years, and all were nonsmokers. Cells were exposed to the peptide N-formylmethionylphenylalanine (F-Met-Phe), zymosan, UICC crocidolite asbestos or latex beads. Oxidant production was measured by luminol-amplified chemiluminescence. Species differed. Peak responses of mouse and hamster macrophages were 1/50 of those of human cells and 1/7 of those of rat and guinea pig cells. Guinea pig cells responded to all agents. Rat cells responded only to zymosan and asbestos. Asbestos was the most effective stimulant for rabbit cells. Cells from cystic fibrosis patients had high basal levels and responded more to F-Met-Phe than to zymosan or asbestos. Peak light came 1-3 min after peptide and 8-140 min after particles. Cells made unresponsive by one stimulus still responded to the other. Omitting calcium and magnesium inhibited the asbestos and latex responses by 92% and 100%, but the F-Met-Phe response by only 52%. The authors concluded that more than one pathway can activate the oxidant-producing burst of alveolar macrophages.

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In plain English

This laboratory study examined alveolar macrophages, which are immune cells washed out of the lungs. The cells came from guinea pigs, rabbits, rats, mice and hamsters, and from patients undergoing lung lavage who had cystic fibrosis, alveolar proteinosis or other lung diseases. The authors measured oxidant production, detected as emitted light, after adding a peptide (F-Met-Phe), a microbial particle (zymosan) or crocidolite asbestos. Responses differed by species. Rat cells responded to zymosan and asbestos but not to the peptide. Asbestos was the most effective stimulant for rabbit cells. Cells from cystic fibrosis patients generally responded more to the peptide than to zymosan or asbestos. In guinea pig cells, peptide responses peaked in 1-3 minutes and particle responses in 8-140 minutes. Cells that no longer responded to one kind of stimulus still responded to the other. Removing calcium and magnesium reduced the asbestos response by 92 percent and the latex bead response by 100 percent, but the peptide response by only 52 percent. The authors concluded that more than one pathway can activate oxidant production in these cells. They noted that the human cells did not come from healthy donors.

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: Laboratory (in vitro) experiment on lung lavage cells from animals and human patients, measuring oxidant production by luminol-amplified chemiluminescence
• Who was studied: Alveolar macrophages from guinea pigs, rabbits, rats, mice and hamsters (5 animals per species in Figure 1, 3 for rabbit). Also human lavage cells from patients at Duke Medical Center: therapeutic lavage of patients with cystic fibrosis and alveolar proteinosis, plus small samples from exploratory lavage of patients with pneumonia, lung cancer, asthma and bronchitis. The patients were aged 8 days to 58 years, and all were nonsmokers. No overall count by diagnosis is given.
• Exposure: Cells were exposed to crocidolite asbestos (UICC standard), zymosan and latex particles (1 mg/ml for particles), and to the peptide N-formylmethionylphenylalanine (F-Met-Phe).
• Main results:
  • Maximally stimulated mouse and hamster alveolar macrophages gave chemiluminescent responses 1/50 of those achievable by human cells and 1/7 of those seen in rat and guinea pig cells.
  • Compared with basal levels, light intensity increased 2-8 fold in cells from mice and hamsters and 24-50 fold in cells from rabbits, rats and guinea pigs.
  • Asbestos was the most effective stimulant for rabbit alveolar macrophages.
  • Rat alveolar macrophages did not respond to F-Met-Phe but were greatly activated by zymosan and asbestos.
  • Cells from cystic fibrosis patients often had high basal levels and were generally more effectively stimulated by F-Met-Phe than by zymosan or asbestos.
  • In guinea pig cells, peak light intensity was reached 1-3 min after peptide addition and 8-140 min after particle addition.
  • Cells stimulated by the peptide could then be stimulated by particles, and vice versa, without washing.
  • When calcium and magnesium were omitted, responses of guinea pig cells to asbestos and latex were inhibited by 92 percent and 100 percent respectively, while the F-Met-Phe response was inhibited by only 52 percent.
• The authors' conclusion: The authors concluded that their results give evidence that more than one pathway is available for activating the oxidant-producing burst of alveolar macrophages.
• Limitations the authors state:
  • The human alveolar macrophages were not obtained from healthy donors.
  • The authors noted that the high basal levels and low responsiveness to particles in cells from cystic fibrosis patients could be due to an unknown particle present in the cell suspensions.

Topics

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Fibrosis, Lung Cancer, UICC, Crocidolite, Macrophage.

Related studies

• Stimulation of oxidant production in alveolar macrophages by pollutant and latex particles — G.E. Hatch, D.E. Gardner, et al. (1980)
• Asbestos effects on superoxide production. An in vitro study of hamster alveolar macrophages — B.W. Case, M.P. Ip, et al. (1986)
• Relative effects of asbestos and wollastonite on alveolar macrophages — W.H. Pailes, D.J. Judy, et al. (1984)
• Effects of asbestos on the random migration of rabbit alveolar macrophages — Q.N. Myrvik, E.A. Knox, et al. (1985)
• Degradation of cartilage proteoglycan and collagen by synovial cells. Stimulation by macrophages under activation by phagocytosis, lymphocyte factors, bacterial products or other inflammatory stimuli — C. Peeters-Joris, G. Vaes (1984)
• In vitro biodegradation of chrysotile fibres by alveolar macrophages and mesothelial cells in culture: comparison with a pH effect — M.C. Jaurand, A. Gaudichet, et al. (1984)

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