Cytokine alteration and speculated immunological pathophysiology in silicosis and asbestos-related diseases

Our plain-English summary of Cytokine alteration and speculated immunological pathophysiology in silicosis and asbestos-related diseases, by S. Murakami, Y. Nishimura, M. Maeda, et al (Environmental Health and Preventive Medicine, 2009).

The study

• Authors: S. Murakami, Y. Nishimura, M. Maeda, N. Kumagai, H. Hayashi, Y. Chen, M. Kusaka, T. Kishimoto, T. Otsuki
• Journal: Environmental Health and Preventive Medicine
• Published: 2009;14(4):216-22
• Cited by: 19 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

This review is partly composed of the presentation "Cytokine alteration and speculated immunological pathophysiology in silicosis and asbestos-related diseases" delivered during the symposium "Biological effects of fibrous and particulate substances and related areas" organized by the Study Group of Fibrous and Particulate Studies of the Japanese Society of Hygiene and held at the 78th Annual Meeting in Kumamoto, Japan. In this review, we briefly introduce the results of recent immunological analysis using the plasma of silica and asbestos-exposed patients diagnosed with silicosis, pleural plaque, or malignant mesothelioma. Thereafter, experimental background and speculation concerning the immunological pathophysiology of silica and asbestos-exposed patients are discussed.

In plain English

This short review, based on a symposium talk by a Japanese research group, presented preliminary plasma cytokine (immune messenger) measurements and the group's earlier laboratory work. Plasma came from 10 healthy donors, 10 silicosis patients (brickyard workers), 15 pleural plaque patients and 8 malignant mesothelioma patients. Reported jobs included shipbuilding, asbestos fiber manufacture and furnace installation, though not every plaque patient's job was listed. IL-6 differed significantly, with mesothelioma patients higher than the other groups. IFN-gamma tended to be lower in mesothelioma patients; no statistical significance was reported for this. Silicosis patients showed no particular change in the measured cytokines, though the group had earlier reported raised antinuclear antibody titers and soluble Fas in silicosis. In a human T-cell line, temporary higher-dose chrysotile exposure killed cells. Low-dose continuous exposure for more than eight months instead produced resistance to asbestos-induced cell death. These resistant cells made more IL-10 and less IFN-gamma, TNF-alpha and IL-6. The authors speculated that asbestos might disrupt immune defenses against tumors during the long latent period. They called their patient data preliminary and said raised IL-6 might partly reflect the cancer itself.

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: Mini-review based on a symposium presentation, combining preliminary plasma cytokine measurements in patients with a summary of the group's earlier cell-line (in vitro) experiments
• Who was studied: 10 healthy donors, 10 silicosis patients (brickyard workers from Bizen City, Okayama prefecture, Japan), 15 pleural plaque patients and 8 malignant mesothelioma patients (plaque and mesothelioma patients diagnosed at Okayama Rosai Hospital, Okayama, Japan); no study dates given
• Exposure: Silicosis patients: brickyard work with free silica estimated at 40–60% in the work environment. Pleural plaque and mesothelioma patients: reported occupations were shipbuilding (3 PP, 5 MM), making asbestos fibers (5 PP, 1 MM), chemical industries (3 PP), construction (1 PP) and furnace installation (2 MM). Adding these up gives all 8 MM patients but only 12 of the 15 PP patients. Fiber type for patients was not stated. Cell experiments: chrysotile at relatively high doses (25–50 micrograms per ml, temporary) or low dose (5–10 micrograms per ml, continuous for more than 8 months)
• Main results:
  • In plasma, significant differences were found for IL-6; mesothelioma patients had higher IL-6 than the other groups (no numeric values given in the text)
  • IFN-gamma tended to be lower in mesothelioma patients than in healthy donors (described as a tendency; no statistical significance reported)
  • Silicosis patients showed no particular change in the measured plasma cytokines
  • The group had previously reported an increase of antinuclear antibody titer and soluble Fas in silicosis (earlier findings, not this study's measurements)
  • In the group's earlier T-cell line experiments, MT-2 cells died by apoptosis after temporary exposure to chrysotile at relatively high doses (25–50 micrograms per ml)
  • By contrast, low-dose (5–10 micrograms per ml) continuous chrysotile exposure for more than 8 months led MT-2 cells to become resistant to asbestos-induced cell death (apoptosis)
  • The chrysotile-exposed subline (CB-1) produced more IL-10 and secreted less IFN-gamma, TNF-alpha and IL-6 than the original MT-2 cells
• The authors' conclusion: The authors speculated that, at some point during the long latent period after asbestos exposure, tumor immunity in exposed people may be disrupted, allowing rapid tumor growth
• Limitations the authors state:
  • The patient data were preliminary and need measurements from more patients
  • Differences from the group's earlier IL-10 finding might be due to the small number of subjects
  • The higher IL-6 in mesothelioma may reflect cancer-related change as well as a direct effect of asbestos
  • It is not certain whether the genetic changes in the CB-1 cells were caused by asbestos exposure

Topics

Medical terms in this study, explained in our Lexicon: Cytokine, Silicosis, Pleural Plaques, Malignant Mesothelioma.

Related studies

• Immunological alterations found in mesothelioma patients and supporting experimental evidence — Y. Miura, Y. Nishimura, et al. (2008)
• Immunological changes in mesothelioma patients and their experimental detection — M. Maeda, Y. Miura, et al. (2008)
• Asbestos-induced cellular and molecular alteration of immunocompetent cells and their relationship with chronic inflammation and carcinogenesis — H. Matsuzaki, M. Maeda, et al. (2012)
• Alteration of cytoskeletal molecules in a human T cell line caused by continuous exposure to chrysotile asbestos — M. Maeda, Y. Chen, et al. (2013)
• Reduction of CXC chemokine receptor 3 in an in vitro model of continuous exposure to asbestos in a human T-cell line, MT-2 — M. Maeda, Y. Nishimura, et al. (2011)
• Decreased CXCR3 expression in CD4+ T cells exposed to asbestos or derived from asbestos-exposed patients — M. Maeda, Y. Nishimura, et al. (2011)

Browse more research in Environmental Health and Preventive Medicine, or return to medical research.