Inflammatory alteration of human t cells exposed continuously to asbestos

Naoko Kumagai-Takei, Shoko Yamamoto, Suni Lee, Megumi Maeda, Hidenori Masuzzaki, Nagisa Sada, Min Yu, Kei Yoshitome, Yasumitsu Nishimura, Takemi Otsuki

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

Asbestos is a known carcinogen and exposure can lead to lung cancer and malignant mesothelioma. To examine the effects of asbestos fibers on human immune cells, the human T cell leukemia/lymphoma virus (HTLV)-1 immortalized human T cell line MT-2 was employed. Following continuous exposure to asbestos fibers for more than eight months, MT-2 sublines showed acquisition of resistance to asbestos-induced apoptosis with decreased death signals and increased surviving signals. These sublines showed various characteristics that suggested a reduction in anti-tumor immunity. On the other hand, inflammatory changes such as expression of MMP7, CXCR5, CXCL13 and CD44 was found to be markedly higher in sublines continuously exposed to asbestos compared with original MT-2 cells. All of these molecules contribute to lung inflammation, T and B cell interactions and connections between mesothelial cells and T cells. Thus, further investigation focusing on these molecules may shed light on the role of chronic inflammation caused by asbestos exposure and the occurrence of malignant mesothelioma. Finally, regarding peripheral T cells from healthy donors (HD) and asbestos-exposed patients with pleural plaque (PP) or malignant pleural mesothelioma (MPM), following stimulation of CD4+ T cells, T cells from MPM patients showed reduced potential of interferon (IFN)-γ expression. Moreover, levels of interleukin (IL)-6, one of the most important cytokines in chronic inflammation, in cultured supernatants were higher in PP and MPM patients compared with HD. Overall, asbestos-induced chronic inflammation in the lung as well as the pleural cavity may facilitate the onset of asbestos-induced cancers due to alterations in the interactions among fibers, immune cells such as T and B cells and macrophages, and mesothelial and lung epithelial cells. Further investigations regarding chronic inflammation caused by asbestos fibers may assist in identifying molecular targets for preventive and therapeutic strategies related to the effects of asbestos exposure.

Original languageEnglish
Article number504
JournalInternational Journal of Molecular Sciences
Volume19
Issue number2
DOIs
Publication statusPublished - Feb 8 2018

Fingerprint

asbestos
Asbestos
T-cells
cells
T-Lymphocytes
lungs
fibers
Fibers
Inflammation
Pneumonia
B-Lymphocytes
cancer
Cells
Tissue Donors
interferon
carcinogens
Deltaretrovirus
Interferons
interleukins
Pleural Cavity

Keywords

  • Apoptosis
  • Asbestos
  • Cell surface molecule
  • IL-6
  • Inflammation
  • Interferon-γ
  • T cell

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

Inflammatory alteration of human t cells exposed continuously to asbestos. / Kumagai-Takei, Naoko; Yamamoto, Shoko; Lee, Suni; Maeda, Megumi; Masuzzaki, Hidenori; Sada, Nagisa; Yu, Min; Yoshitome, Kei; Nishimura, Yasumitsu; Otsuki, Takemi.

In: International Journal of Molecular Sciences, Vol. 19, No. 2, 504, 08.02.2018.

Research output: Contribution to journalReview article

Kumagai-Takei, N, Yamamoto, S, Lee, S, Maeda, M, Masuzzaki, H, Sada, N, Yu, M, Yoshitome, K, Nishimura, Y & Otsuki, T 2018, 'Inflammatory alteration of human t cells exposed continuously to asbestos', International Journal of Molecular Sciences, vol. 19, no. 2, 504. https://doi.org/10.3390/ijms19020504
Kumagai-Takei, Naoko ; Yamamoto, Shoko ; Lee, Suni ; Maeda, Megumi ; Masuzzaki, Hidenori ; Sada, Nagisa ; Yu, Min ; Yoshitome, Kei ; Nishimura, Yasumitsu ; Otsuki, Takemi. / Inflammatory alteration of human t cells exposed continuously to asbestos. In: International Journal of Molecular Sciences. 2018 ; Vol. 19, No. 2.
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AU - Lee, Suni

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AU - Sada, Nagisa

AU - Yu, Min

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