Studies on the fate of pulmonary surfactant in the lung

Our plain-English summary of Studies on the fate of pulmonary surfactant in the lung, by R. Desai, T.D. Tetley, C.G. Curtis, et al (The Biochemical Journal, 1978).

The study

• Authors: R. Desai, T.D. Tetley, C.G. Curtis, G.M. Powell, R.J. Richards
• Journal: The Biochemical Journal
• Published: 1978;176(2):455-62
• Cited by: 52 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

1. Radioactively labelled pulmonary surfactant was prepared in an isolated perfused lung system provided with [14C]hexadecanoate. 2. After intratracheal administration of pulmonary surfactant radioactively labelled components were rapidly distributed into different lung fractions, including macrophages (free cells), but most of the radioactive label was accumulated by the lung tissue. 3. Alveolar macrophages, maintained in a variety of culture media in the presence and absence of mineral particles, incorporated a low percentage (11%) of radioactively labelled components when incubated with the surfactant, although evolution of labelled CO2 (6% of the original total activity) suggested that some breakdown of the components had taken place. 4. In similar cultures little intracellular accumulation or extracellular release of non-esterified fatty acids was demonstrated, indicating minimal catabolism of the high-molecular-weight lipid components of surfactant (particularly phosphatidylcholine). 5. However, experiments in vitro designed to simulate the lysosomal degradation of endocytosed surfactant indicated that the macrophage had enzymes capable of releasing non-esterified fatty acids, particularly hexadecanoate, from the lipoprotein complex. 6. It is argued that lung cells, other than alveolar macrophages, may also have a role in surfactant turnover.

In plain English

This laboratory study in rabbits and sheep examined the fate of pulmonary surfactant, the fatty material lining the lung's air sacs, and whether alveolar macrophages (scavenger cells) break it down. The authors made radioactively labelled surfactant in isolated rabbit lungs, then placed it into the lungs of live rabbits. After 1 hour, 57% of the injected label was detected in the lungs, and about 30% of that detected label was in the surfactant. Of the detected label, lung tissue held 32% at 1 hour and 52% at 8 hours, and free lung cells 16% and 8%; recovery fell to 49.5%. In cultures, 13-16% of the label became associated with rabbit macrophages, with 7-11% inside the cells. Brazilian silica or Chrysotile A asbestos had a negligible effect on this. An enzyme preparation from sheep macrophages released fatty acids from surfactant, unaffected by chrysotile, but converted only 10% of the surfactant to fatty acids after 22 hours. The authors concluded that macrophages did not appear to contribute significantly to surfactant digestion and that other lung cells may play a role. They noted that their test-tube systems were artificial.

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 animal experiment: isolated perfused rabbit lungs, intratracheal injection in live rabbits (in vivo), cultured alveolar macrophages and a lysosomal enzyme preparation (in vitro)
• Who was studied: Mature male Dutch rabbits (used in most experiments; numbers of animals not stated) and sheep lungs obtained from a slaughterhouse; Cardiff, Wales
• Exposure: Radioactively labelled pulmonary surfactant; in cultures, UICC Rhodesian Chrysotile A asbestos or Brazilian silica at 100 micrograms of mineral per ml; 20 mg chrysotile in the enzyme study
• Main results:
  • In live rabbits, 57% of the injected label was detectable in lung fractions 1 hour after injection
  • In live rabbits, recovery of the injected label in lung fractions decreased with time (Table 3: 49.5% at 8 hours)
  • In live rabbits, 1 hour after injection, about 30% of the detected radioactivity was associated with the pulmonary surfactant (Table 3 gives 28.7% of detectable radioactivity), and this value was maintained throughout the experiment
  • In live rabbits, lung tissue (after lavage) held 32% of the detected label at 1 hour
  • In live rabbits, the lung tissue share of the detected label increased to 52% within 8 hours
  • In live rabbits, the free cell population (macrophages) held 16% of the detected label at 1 hour, falling to 8% at 8 hours
  • In live rabbits, 2 hours after injection, 48% of the label in the pulmonary surfactant was in phosphatidylcholine, compared with 73% in the original material; the proportion in non-esterified fatty acids increased
  • In cultured normal rabbit alveolar macrophages given labelled surfactant, 13-16% of the label was associated with the cells
  • Of the label associated with these cultured macrophages, 7-11% was located inside the cells
  • In cultured macrophages given free labelled hexadecanoate instead, about 50% of the label was associated with the cells
  • In macrophage cultures, the presence of silica dust or chrysotile asbestos had a negligible effect on the distribution of label from the surfactant
  • A lysosomal enzyme preparation from sheep alveolar macrophages released non-esterified fatty acids and hexadecanoate from sheep surfactant in a time-dependent way, and chrysotile asbestos did not interfere
  • In the lysosomal enzyme system, only 10% of the available surfactant was degraded to non-esterified fatty acids after 22 hours
• The authors' conclusion: The authors concluded that alveolar macrophages did not appear to contribute significantly to digestion of the labelled surfactant, and that alveolar cells other than macrophages (Type I and Type II) may also have a role in removing surfactant components
• Limitations the authors state:
  • The authors stated that both test-tube systems were artificial: the enzyme study maximized contact between surfactant and enzymes, and the cell cultures could not reproduce conditions in the living lung
  • The authors stated that it was difficult to assess whether the alveolar macrophage is the main cell responsible for surfactant breakdown
  • The authors stated that the distribution of label in surfactant preparations was not always identical between preparations
  • The authors stated that further studies are needed to determine the turnover rate of surfactant

Topics

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

Related studies

• Chrysotile-induced asbestosis: changes in the free cell population, pulmonary surfactant and whole lung tissue of rats — T.D. Tetley, P.M. Hext, et al. (1976)
• Changes in pulmonary surfactant and phosphatidylcholine metabolism in rats exposed to chrysotile asbestos dust — T.D. Tetley, R.J. Richards, et al. (1977)
• Effect of air pollutants on the pulmonary surfactant system — B. Müller, C. Seifart, et al. (1998)
• Changes in surfactant in bronchoalveolar lavage fluid after hemithorax irradiation in patients with mesothelioma — M. Hallman, P. Maasilta, et al. (1990)
• Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers — O. Lesur, A.M. Bernard, et al. (1996)
• Lung surfactant protein-A and carcinoembryonic antigen in pleural effusions due to lung adenocarcinoma and malignant mesothelioma — N. Shijubo, Y. Honda, et al. (1995)

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