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Int. J. Mol. Sci. 2018, 19(2), 504; doi:10.3390/ijms19020504

Inflammatory Alteration of Human T Cells Exposed Continuously to Asbestos

1
Department of Hygiene, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan
2
Department of Biofunctional Chemistry, Division of Bioscience, Okayama University Graduate School of Natural Science and Technology, 1-1-1 Tsushima-Naka, Kita-Ku, Okayama 700-8530, Japan
3
Department of Life Science, Faculty of Life and Environmental Science, Prefectural University of Hiroshima, Shobara, Hiroshima 727-0023, Japan
4
Department of Biophysical Chemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8530, Japan
5
Department of Occupational and Environmental Health Science, School of Public Health, Peking University, 38 Xueyuan Road, Beijing 100191, China
6
Department of Occupational Diseases, Zhejiang, Academy of Medical Sciences, 182 Tian Mu Shan Road, Zhejiang 310013, China
*
Author to whom correspondence should be addressed.
Received: 4 January 2018 / Revised: 5 February 2018 / Accepted: 6 February 2018 / Published: 8 February 2018
(This article belongs to the Special Issue Macrophages in Inflammation)
View Full-Text   |   Download PDF [866 KB, uploaded 8 February 2018]   |  

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. View Full-Text
Keywords: asbestos; T cell; apoptosis; inflammation; cell surface molecule; IL-6; interferon-γ asbestos; T cell; apoptosis; inflammation; cell surface molecule; IL-6; interferon-γ
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Kumagai-Takei, N.; Yamamoto, S.; Lee, S.; Maeda, M.; Masuzzaki, H.; Sada, N.; Yu, M.; Yoshitome, K.; Nishimura, Y.; Otsuki, T. Inflammatory Alteration of Human T Cells Exposed Continuously to Asbestos. Int. J. Mol. Sci. 2018, 19, 504.

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