Immunological alterations found in mesothelioma patients and supporting experimental evidence

Our plain-English summary of Immunological alterations found in mesothelioma patients and supporting experimental evidence, by Y. Miura, Y. Nishimura, M. Maeda, et al (Environmental Health and Preventive Medicine, 2008).

The study

• Authors: Y. Miura, Y. Nishimura, M. Maeda, S. Murakami, H. Hayashi, K. Fukuoka, T. Kishimoto, T. Nakano, T. Otsuki
• Journal: Environmental Health and Preventive Medicine
• Published: 2008;13(2):55-9
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

It is common knowledge that exposure to asbestos causes asbestos-related diseases, such as asbestosis, lung cancer and malignant mesothelioma, not only in people who have had long-term contact with asbestos in their work environment but also in residents living near factories that handle asbestos. Since the summer of 2005, these revelations turned into a large medical problem and caused and social unrest. We have focused on the immunological effects of both asbestos and silica on the human immune system. In this brief review, we introduce immunological alterations found in patients with malignant mesothelioma and describe the experimental background in which these were found. Analyzing the immunological effects of asbestos may improve our understanding of the biological effects of asbestos.

In plain English

This was a brief review in which the authors described their own laboratory and clinical findings on how asbestos may affect the human immune system. In experiments, mostly with chrysotile asbestos, a human T-cell line called MT-2 underwent apoptosis (cell death) after short-term, high-dose chrysotile exposure. A subline made resistant to this cell death showed increased bcl-2, excessive IL-10 and STAT3 activation. Peripheral CD4+ T cells from malignant mesothelioma patients expressed significantly more bcl-2 than those from healthy volunteers and asbestosis patients. In mesothelioma patients, a statistical factor analysis grouped bcl-2 level, past asbestos exposure, platelet count and serum CRP together. Six healthy volunteers, nine asbestosis patients and 12 mesothelioma patients were compared. In the patients, various T cell receptor Vbeta types were overexpressed, and Vbeta1, 4 and 9 were strongly overexpressed in many of them. The authors concluded that asbestos affects immune cells and that these effects may be associated with complications such as malignant tumors. They noted the patient data were limited and that further study was needed.

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: Brief review of the authors' own experimental (cell line) and clinical immunological findings
• Who was studied: A human T-cell line (MT-2) and a chrysotile-resistant subline (MT-2Rst). For the T cell receptor analysis: six healthy volunteers, nine asbestosis patients (all male) and 12 malignant mesothelioma patients (9 male, 3 female), Japan. Group sizes for the bcl-2 comparison are not given.
• Exposure: Chrysotile asbestos in laboratory experiments: short-term high-dose exposure, and long-term low-dose exposure. Patients' past asbestos exposure was also examined.
• Main results:
  • Peripheral CD4+ T cells from malignant mesothelioma patients expressed significantly more bcl-2 than those of healthy volunteers and asbestosis patients (finding from the authors' earlier study).
  • Short-term, high-dose chrysotile exposure caused apoptosis in the MT-2 T-cell line.
  • The chrysotile-induced apoptosis-resistant subline MT-2Rst showed enhanced bcl-2 expression, excessive IL-10 secretion and expression, and STAT3 activation.
  • In mesothelioma patients, factor analysis grouped bcl-2 relative expression in CD4+ T cells (0.59009), past asbestos exposure (0.55496), platelet count (-0.76064) and serum CRP (-0.79789) into one factor, with a contribution rate of 19.18%.
  • Various T cell receptor Vbeta types were overexpressed in mesothelioma and asbestosis patients. Vbeta1, 4 and 9, among 24 types, were strongly overexpressed in many patients.
  • MT-2Rst cells overexpressed various T cell receptor Vbeta types and showed no significant changes when they again came in contact with chrysotile.
• The authors' conclusion: The authors concluded that asbestos affects immunocompetent cells and that these effects may be associated with complications such as malignant tumors in asbestos-exposed patients. They suggested that multiple T cell receptor Vbeta overexpression may be a candidate marker for detecting prior asbestos exposure.
• Limitations the authors state:
  • Further study is needed to determine whether patients with other cancers show the same bcl-2 change.
  • The T cell receptor data came from a limited number of patients.

Topics

Medical terms in this study, explained in our Lexicon: Mesothelioma, Lung Cancer, Malignant Mesothelioma.

Related studies

• Immunological changes in mesothelioma patients and their experimental detection — M. Maeda, Y. Miura, et al. (2008)
• Cytokine alteration and speculated immunological pathophysiology in silicosis and asbestos-related diseases — S. Murakami, Y. Nishimura, et al. (2009)
• 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- — T. Otsuki, Y. Miura, et al. (2007)
• Functional Alteration of Natural Killer Cells and Cytotoxic T Lymphocytes upon Asbestos Exposure and in Malignant Mesothelioma Patients — Y. Nishimura, N. Kumagai-Takei, et al. (2015)
• Asbestos-induced cellular and molecular alteration of immunocompetent cells and their relationship with chronic inflammation and carcinogenesis — H. Matsuzaki, M. Maeda, et al. (2012)
• Evidence supporting a role for active oxygen species in asbestos-induced toxicity and lung disease — B.T. Mossman, J.P. Marsh (1989)

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