Immunological Effects of Silica and Related Dysregulation of Autoimmunity

Kumagai, Naoya; Hayashi, Hiroaki; Maeda, Megumi; Miura, Yoshie; Matsuzaki, Hidenori; Lee, Sai Peck; Nishimura, Yasumasa; Fujimoto, Wataru; Otsuki, Takemi

doi:10.5772/19218

Cited by 8 publications

(7 citation statements)

References 96 publications

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“…More recently, attention has been paid to the role of silica in autoimmune responses, in which autoimmune cells are activated by signals from silica-induced apoptotic macrophages (141). Following silica exposure, Tregs and Responder T cells (Tresps) are chronically activated and infiltrate the peripheral T cell population.…”

Section: Adaptive Cellular Immune Responses In Silicosis and Tuberculmentioning

confidence: 99%

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

et al. 2019

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Exposure to silica and the consequent development of silicosis are well-known health problems in countries with mining and other dust producing industries. Apart from its direct fibrotic effect on lung tissue, chronic and immunomodulatory character of silica causes susceptibility to tuberculosis (TB) leading to a significantly higher TB incidence in silica-exposed populations. The presence of silica particles in the lung and silicosis may facilitate initiation of tuberculous infection and progression to active TB, and exacerbate the course and outcome of TB, including prognosis and survival. However, the exact mechanisms of the involvement of silica in the pathological processes during mycobacterial infection are not yet fully understood. In this review, we focus on the host's immunological response to both silica and Mycobacterium tuberculosis, on agents of innate and adaptive immunity, and particularly on silica-induced immunological modifications in co-exposure that influence disease pathogenesis. We review what is known about the impact of silica and Mycobacterium tuberculosis or their co-exposure on the host's immune system, especially an impact that goes beyond an exclusive focus on macrophages as the first line of the defense. In both silicosis and TB, acquired immunity plays a major role in the restriction and/or elimination of pathogenic agents. Further research is needed to determine the effects of silica in adaptive immunity and in the pathogenesis of TB.

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Section: Adaptive Cellular Immune Responses In Silicosis and Tuberculmentioning

confidence: 99%

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

et al. 2019

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“…Fas-mediated apoptosis may proceed more easily in the latter fraction due to various stimuli by self-or foreign antigens or the anti-Fas autoantibody, which we discovered in the serum of silicosis patients, and repeated recruitment from the bone marrow. Peripheral T cells derived from silicosis patients were shown to be the dominant sFas producer with a smaller fraction of apoptosis-prone T cells than that from healthy donors [25][26][27]. The sFas-producing fraction may survive longer and retain a chronically activated status.…”

Section: Immune Response Activationmentioning

confidence: 99%

“…We previously investigated the immunological effects of silica using human peripheral blood immune cells derived from healthy donors and silicosis patients [25][26][27]. In this review, we summarized our findings, in which silica was shown to be an environmental immunostimulator and the chronic activation of immune cells by recurrent and chronic exposure to silica was demonstrated to cause an imbalance in the regulation of T cell responses.…”

Section: Introductionmentioning

confidence: 99%

Immunostimulation by Silica Particles and the Development of Autoimmune Dysregulation

Lee¹,

Hayashi²,

Maeda³

et al. 2014

Immune Response Activation

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“…These activations induce overexpression of CD95/Fas in Treg, resulting in early loss and contamination of activated Tresp, which express CD25 as the marker for activation into a peripheral CD4+25+ subpopulation of T cells. These phenomena seem to induce reduced regulation of autoimmunity [ 37 , 38 ]. Regarding silica-induced fibrosis (lung and skin), the idea proposed previously [ 27 ] is that silica affect alveolar macrophages, endothelial cells, and fibroblasts to modify cytokine production and disturbance of collagen synthesis and degradation, subsequently forming fibrosis of lung and skin lesion.…”

Section: Immunological Effects Of the Mineral Silicate On Asbestosmentioning

confidence: 99%

Asbestos-Induced Cellular and Molecular Alteration of Immunocompetent Cells and Their Relationship with Chronic Inflammation and Carcinogenesis

Matsuzaki

Maeda

Lee

et al. 2012

Journal of Biomedicine and Biotechnology

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Asbestos causes lung fibrosis known as asbestosis as well as cancers such as malignant mesothelioma and lung cancer. Asbestos is a mineral silicate containing iron, magnesium, and calcium with a core of SiO2. The immunological effect of silica, SiO2, involves the dysregulation of autoimmunity because of the complications of autoimmune diseases found in silicosis. Asbestos can therefore cause alteration of immunocompetent cells to result in a decline of tumor immunity. Additionally, due to its physical characteristics, asbestos fibers remain in the lung, regional lymph nodes, and the pleural cavity, particularly at the opening sites of lymphatic vessels. Asbestos can induce chronic inflammation in these areas due to the production of reactive oxygen/nitrogen species. As a consequence, immunocompetent cells can have their cellular and molecular features altered by chronic and recurrent encounters with asbestos fibers, and there may be modification by the surrounding inflammation, all of which eventually lead to decreased tumor immunity. In this paper, the brief results of our investigation regarding reduction of tumor immunity of immunocompetent cells exposed to asbestosin vitroare discussed, as are our findings concerned with an investigation of chronic inflammation and analyses of peripheral blood samples derived from patients with pleural plaque and mesothelioma that have been exposed to asbestos.

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Immunological Effects of Silica and Related Dysregulation of Autoimmunity

Cited by 8 publications

References 96 publications

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

Immunostimulation by Silica Particles and the Development of Autoimmune Dysregulation

Asbestos-Induced Cellular and Molecular Alteration of Immunocompetent Cells and Their Relationship with Chronic Inflammation and Carcinogenesis

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