Keynote lecture in the 13th Japanese Society of Immunotoxicology (JSIT 2006) : -Pathophysiological Development and Immunotoxicology: what we have found from research related to silica and silicate such as asbestos-

Our plain-English summary of Keynote lecture in the 13th Japanese Society of Immunotoxicology (JSIT 2006) : -Pathophysiological Development and Immunotoxicology: what we have found from research related to silica and silicate such as asbestos-, by T. Otsuki, Y. Miura, M. Maeda, et al (Environmental Health and Preventive Medicine, 2007).

The study

• Authors: T. Otsuki, Y. Miura, M. Maeda, H. Hayashi, S. Murakami, M. Dong, Y. Nishimura
• Journal: Environmental Health and Preventive Medicine
• Published: 2007;12(4):153-60
• Cited by: 2 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Silica and silicates may disturb immune functions such as autoimmunity and tumor immunity, because people who are exposed to the materials sometimes develop autoimmune and malignant diseases, respectively. Although silica-induced disorders of autoimmunity have been explained as adjuvant-type effects of silica, more precise analyses are needed and should reflect the recent progress in immunomolecular findings. A brief summary of our investigations related to the immunological effects of silica/asbestos is presented. Recent advances in immunomolecular studies led to detailed analyses of the immunological effects of asbestos and silica. Both affect immuno-competent cells and these effects may be associated with the pathophysiological development of complications in silicosis and asbestos-exposed patients such as the occurrence of autoimmune disorders and malignant tumors, respectively. In addition, immunological analyses may lead to the development of new clinical tools for the modification of the pathophysiological aspects of diseases such as the regulation of autoimmunity or tumor immunity using cell-mediated therapies, various cytokines, and molecule-targeting therapies. In particular, as the incidence of asbestos-related malignancies is increasing and such malignancies have been a medical and social problem since the summer in 2005 in Japan, efforts should be focused on developing a cure for these diseases to eliminate the nation wide anxiety about these malignancies.

In plain English

This article was a review, based on a keynote lecture, of the authors' own earlier studies on how crystalline silica and asbestos affect immune cells. It reported no new data or patient numbers. Compared with healthy donors, silicosis patients had higher blood levels of soluble Fas, a molecule involved in controlling immune-cell death. Antibodies against Fas and caspase-8 were frequent in their serum. A blood T cell fraction including regulatory T cells was slightly below its age-predicted share from healthy donors and worked less well. For asbestos, they described chrysotile experiments on MT-2, a human T cell line. High-level, short-term exposure caused cell death. A subline resistant to chrysotile-B showed more bcl-2 and IL-10. The authors called higher bcl-2 in CD4+ blood T cells from patients with malignant mesothelioma, versus asbestosis patients or healthy donors, partial confirmation of this. They concluded these effects may be associated with autoimmune disorders in silicosis and malignant tumors in asbestos-exposed patients. They wrote that possible asbestos effects on natural killer and regulatory T cells, and mesothelioma cells' effects on immune cells, were mostly unclarified.

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: Minireview (keynote lecture) summarizing the authors' own previously published investigations; no new data presented
• Who was studied: In the summarized earlier studies: silicosis patients compared with healthy donors, and patients with asbestos-related diseases (asbestosis and malignant mesothelioma) compared with silicosis patients and healthy donors, plus a human T cell line (MT-2). No numbers, places or dates are given in this article.
• Exposure: Crystalline silica (in silicosis patients and in cell culture) and asbestos, in particular chrysotile (chrysotile-A and chrysotile-B) applied to cells in culture, both short-term high-dose and long-term low-dose
• Main results:
  • In silicosis patients, serum soluble Fas was higher than in healthy donors (from the authors' earlier study)
  • Antibodies against Fas and caspase-8 were frequently detected in serum from silicosis patients
  • The share of the CD4+25+ T cell fraction, which includes regulatory T cells, was slightly lower in silicosis patients than the age-predicted value from healthy donors
  • The function of this CD4+25+ fraction in silicosis patients was weaker than in healthy donors, as measured by mixed lymphocyte reaction analysis
  • In the authors' earlier work, asbestos activated CD4+ T cells and caused activation-induced cell death
  • MT-2 T cells exposed to chrysotile at high level for a short time underwent apoptosis (cell death)
  • A subline of MT-2 cells resistant to chrysotile-B-induced cell death showed excessive IL-10 secretion and expression, along with enhanced bcl-2 expression
  • CD4+ peripheral blood T cells from patients with malignant mesothelioma showed higher bcl-2 expression than those from patients with asbestosis or healthy donors, which the authors described as partial confirmation of their proposed mechanism
  • Patients with asbestos-related diseases showed a limited overexpression of T cell receptor Vbeta without clonal expansion; silicosis patients showed a significant overexpression of TcRVbeta 7.2
• The authors' conclusion: The authors concluded that silica and asbestos affect immune cells and that these effects may be associated with autoimmune disorders in silicosis patients and malignant tumors in asbestos-exposed patients, respectively
• Limitations the authors state:
  • The authors stated that possible effects of asbestos on NK cells and regulatory T cells, and effects of mesothelioma cells on immune cells, are mostly not yet clarified
  • The authors stated that it remains to be clarified why silica exposure leads to more alternative splicing of fas and how it decreases regulatory T cells

Topics

Medical terms in this study, explained in our Lexicon: Silicate, Silicosis, Cytokine.

Related studies

• Expression of the T cell receptor Vbeta repertoire in a human T cell resistant to asbestos-induced apoptosis and peripheral blood T cells from patients with silica and asbestos-related diseases — Y. Nishimura, Y. Miura, et al. (2006)
• Immunological alterations found in mesothelioma patients and supporting experimental evidence — Y. Miura, Y. Nishimura, et al. (2008)
• A hazardous society? Individual versus community responsibility in cancer prevention. Third annual Matthew B. Rosenhaus Lecture — J. Higginson (1976)
• Asbestos and malignant mesothelioma: foreword. Reviews of a symposium entitled "Malignant Mesothelioma" organized by the Study Group on Fibrous and Particulate Substances of the 77th Annual Meeting of the Japanese Society for Hygiene, 2007 — T. Otsuki (2008)
• Screening for lung cancer in a high-risk group: but I still haven't found what I'm looking for — G.A. Silvestri (2007)
• Chrysotile asbestos detoxification with a combined treatment of oxalic acid and silicates producing amorphous silica and biomaterial — A. Valouma, A. Verganelaki, et al. (2016)

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