Immunologic aspects of pneumoconiosis

Our plain-English summary of Immunologic aspects of pneumoconiosis, by R.K. Scheule, A. Holian (Experimental Lung Research, 1991).

The study

• Authors: R.K. Scheule, A. Holian
• Journal: Experimental Lung Research
• Published: 1991;17(4):661-85
• Type of article: Review
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

This review summarizes recent research bearing on the role played by cells of the immune system in the development of pneumoconiosis. Findings related to the cellular and humoral immune responses to silica and asbestos are highlighted. Experimental results from humans and animal models are integrated into our current understandings of cellular and cytokine-mediated pathways leading to the generation of immune responses that may contribute to fibrogenesis and fibrosis. Potential mechanisms leading to the generation of an immune response by particulates are discussed, together with the indirect effects of particulates on fibroblasts by way of the cytokine network in the lung. Finally, suggestions are given for future research to help further elucidate the relationships between the cellular components of the immune system of the lung and the fibroblast that lead to fibrosis.

In plain English

This article was a mini-review, not a new study. The authors summarized published human and animal research on how immune system cells may contribute to pneumoconiosis, the lung scarring caused by inhaled dusts, using asbestos and silica as examples. Studies they cited reported autoantibodies and high antibody levels in patients with asbestosis or silicosis, but studies disagreed on whether these matched the severity of lung scarring on X-rays. One cited study found a subset of asbestos-exposed workers with an abnormal balance of T-cell types. Another found more lymphocytes in lung washings of asbestos-exposed workers without detectable fibrosis than in matched controls. Cited mouse studies found that long crocidolite fibers produced fibrosis while short ones produced virtually none. The authors noted that animal experiments are not perfect models of human exposure, because rodents breathe only through the nose and are typically given higher doses than humans are likely to encounter. The authors concluded that the immune and scarring responses to dust are linked. They also stated that which of the proposed ways particles might trigger immune responses actually operate had not been well established.

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: Narrative review (labeled a mini-review) of published human, animal and laboratory studies
• Who was studied: No study population of its own; the review drew on previously published studies in humans and animal models (rats, mice, sheep)
• Exposure: Asbestos (including chrysotile and crocidolite in cited studies) and silica, used as model fibrogenic dusts; nonfibrogenic dusts such as titanium dioxide discussed for comparison
• Main results:
  • Reviewed studies reported autoantibodies and hypergammaglobulinemia (high antibody levels) in patients with asbestosis and in patients with silicosis
  • Cited studies disagreed: one reported that antinuclear antibody levels correlated with fibrosis on chest radiographs in asbestosis, while a more recent study found no such correlation for any humoral immune measure
  • A cited study (Tsang and coworkers) of workers with occupational asbestos exposure identified a subset (printed as approximately 30%) with a significantly depressed ratio of helper to suppressor T cells
  • A cited study of asbestos-exposed workers without detectable fibrosis found higher lymphocyte concentrations in lung lavage fluid than in matched controls, and this lymphocytosis correlated with pleural abnormalities
  • In cited mouse studies, instilled short crocidolite fibers (length under 2.5 micrometers) produced very few fibers in the lung interstitium and virtually no fibrosis, whereas long crocidolite fibers produced a fibrotic reaction
  • A cited study reported that alveolar macrophages from people with interstitial lung disease caused by asbestos, silica or coal dust appeared activated
  • In a cited sheep model, immune cell responses to mitogens were above normal during the first 6 months of low-dose intratracheal asbestos and depressed by 12 months
• The authors' conclusion: The authors concluded that dividing the lung's response to dust into separate fibrotic and immune responses is artificial because the two are linked. They stated that it has not been well established which of the proposed mechanisms operate in a given pneumoconiosis, and they suggested in vivo animal studies combined with in situ probes.
• Limitations the authors state:
  • Animal exposure methods are not perfect models of human exposure: rodents breathe only through the nose and are typically given higher doses than humans are likely to encounter
  • Overloading the lung with a nuisance dust in experiments can produce a response indistinguishable from that of a fibrogenic dust, which may confuse interpretation
  • The authors noted that the mechanisms they described as possible had not been well established

Topics

Medical terms in this study, explained in our Lexicon: Pneumoconiosis, Cytokine, Fibrosis, Fibroblast.

Related studies

• Asbestos toxicity: an immunologic perspective — G.J. Rosenthal, P. Simeonova, et al. (1999)
• Investigative techniques in the laboratory study of coal workers' pneumoconiosis: recent advances at the cellular level — J.S. Harington (1972)
• Experimental infective pneumoconiosis: effect of asbestos dust and Candida albicans infection on the lungs of rhesus monkeys — S.H. Zaidi, R. Shanker, et al. (1973)
• Impaired chemotactic responses of bronchoalveolar leukocytes in experimental pneumoconiosis — K. Donaldson, G.M. Brown, et al. (1990)
• WHO/ILO work-related burden of disease and injury: Protocol for systematic reviews of occupational exposure to dusts and/or fibres and of the effect of occupational exposure to dusts and/or fibres on pneumoconiosis — D. Mandrioli, V. Schlünssen, et al. (2018)
• "Labrador lung": an unusual mixed dust pneumoconiosis — H.W. Edstrom, D.M. Rice (1982)

Browse more research in Experimental Lung Research, or return to medical research.