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IMMUNOLOGICAL EFFECTS OF ASBESTOS, pp. 175 - 184 $100.00
Authors:  Takemi Otsuki, Megumi Maeda, Yoshie Miura, Hiroaki Hayashi, Shuko Murakami, Naoko Kumagai, and Yasumitsu Nishimura
Abstract:
Asbestos is a class of silicate minerals containing metals such as iron and magnesium.
[1,2] It is divided into two groups: amphiboles, which include crocidolite, amosite and others,
and serpentine, which is only represented by chrysotile. Iron-containing minerals such as
crocidolite and amosite possess stronger carcinogenic activities than chrysotile, and asbestos
causes malignant tumors such as lung cancer and malignant mesothelioma. [3-5] In addition,
asbestos induces fibrogenic changes through pulmonary lesions and causes asbestosis of the
lung. [6,7] The immunological effects of asbestos have not been investigated because an
analysis of the mechanisms concerning the fibrogenic and carcinogenic potential of asbestos
is considered the first step in determining the treatment and prevention of asbestos-related
diseases. [8] However, immunological effects may be important because tumor immunity
plays an important role in the development and progression of cancer cells. In addition, an
evaluation of general immune status may be important for use in immunotherapy, such as
transferring cytotoxic immunocompetent cells that recognize cancer-specific antigens.
The cellular and molecular biological effects of asbestos fibers on alveolar epithelial cells
and/or pleural mesothelial cells have been investigated using various animal models and
culture cells. In regard to fibrogenesis, the initial recognition of asbestos by alveolar
macrophage (AM) has been important and AM-releasing cytokines such as tumor necrosis
factor (TNF)-α, transforming growth factor (TGF)-β, interleukin (IL)-1β and IL-8 play a
critical role in activating mesenchymal cells to induce the proliferation of collagen fibers.
[9,10] Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play important roles in carcinogenesis, [11,12] in which substances that damage DNA are generated through
the activity of iron contained in the asbestos. Alveolar and/or mesothelial cells exposed to
asbestos then develop apoptosis with activation of a mitochondrial pathway and a BAX
dominant balance of the BAX/BCL-2 complex, cytosomal release of cytochrome-c from
mitochondria, and activation of caspase 9 and 3. [11,12]
However, this knowledge is based on studies using animal models and cell culture
experiments in which exposure conditions were temporary and involved high doses. In human
asbestos-related diseases, the latent time is quite long and may range from 10 to 30 years for
fibrogenic changes known as asbestosis, and around 40 years for malignant mesothelioma.
[13]
In order to investigate the immunological effects of asbestos on human
immunocompetent cells, experimental procedures of exposure should more accurately reflect
the conditions associated with this human disease. Therefore, a human T-cell lymphotropic
virus (HTLV) type 1-immortalized human polyclonal T-cell line (MT-2) was utilized in
experiments because this cell line is not tumor-cell derived and is reported to have a normal
karyotype. [14] Additionally, screening for sensitivity to chrysotile-asbestos revealed that the
MT-2 cells and a few Epstein-Barr virus immortalized B lymphoblastoid cell lines were
relatively sensitive (easy to die) in comparison to other T and B cell tumor-derived lines.
Since the theory suggests that the effects on T cells may be more important than those on B
cells regarding the alteration of tumor immunity, MT-2 cells were chosen for in vitro
experiments.
A high dose and temporary exposure were first examined to investigate the effects of
asbestos on alveolar epithelial and pleural mesothelial cells. Low-dose and continuous
exposure models were then developed, and cellular and molecular characteristics of cells
exposed continuously to chrysotile were identified and compared with the original MT-2
cells. We used chrysotile in our series of experiments because it may be important to compare
asbestos with silica (SiO2), which causes silicosis and alteration of autoimmunity. [15,16] In
addition, the dose of chrysotile used in industries around the world is much higher than that of
asbestos, and carcinogenicity is considered much lower for chrysotile. [17,18] Although a
crocidolite-exposure model has been developed, the results obtained from the chrysotileexposure
model will be shown here. 


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IMMUNOLOGICAL EFFECTS OF ASBESTOS, pp. 175 - 184