Immunological effects of silica and asbestos.

Department of Hygiene, Kawasaki Medical School, Matsushima 577, Kurashiki 7010192, Japan.
Cellular & molecular immunology (Impact Factor: 3.42). 09/2007; 4(4):261-8.
Source: PubMed

ABSTRACT Silicosis patients (SILs) and patients who have been exposed to asbestos develop not only respiratory diseases but also certain immunological disorders. In particular, SIL sometimes complicates autoimmune diseases such as systemic scleroderma, rheumatoid arthritis (known as Caplan syndrome), and systemic lupus erythematoses. In addition, malignant complications such as lung cancer and malignant mesothelioma often occur in patients exposed to asbestos, and may be involved in the reduction of tumor immunity. Although silica-induced disorders of autoimmunity have been explained as adjuvant-type effects of silica, more precise analyses are needed and should reflect the recent progress in immunomolecular findings. A brief summary of our investigations related to the immunological effects of silica/asbestos is presented. Recent advances in immunomolecular studies led to detailed analyses of the immunological effects of asbestos and silica. Both affect immuno-competent cells and these effects may be associated with the pathophysiological development of complications in silicosis and asbestos-exposed patients such as the occurrence of autoimmune disorders and malignant tumors, respectively. In addition, immunological analyses may lead to the development of new clinical tools for the modification of the pathophysiological aspects of diseases such as the regulation of autoimmunity or tumor immunity using cell-mediated therapies, various cytokines, and molecule-targeting therapies. In particular, as the incidence of asbestos-related malignancies is increasing and such malignancies have been a medical and social problem since the summer of 2005 in Japan, efforts should be focused on developing a cure for these diseases to eliminate nationwide anxiety.

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    ABSTRACT: Silica particles and asbestos fibers, which are known as typical causatives of pneumoconiosis, induce lung fibrosis. Moreover, silicosis patients often complicate with autoimmune diseases, and asbestos-exposed patients suffer from malignant diseases such as pleural mesothelioma and lung cancer. We have been conducting experimental studies to investigate altered regulation of self-tolerance caused by silica exposure, including analyses using specimens such as plasma and immunocompetent cells obtained from silicosis patients, as a means of examining the supposition that silica exposure induces molecular and cellular biological alterations of immune cells. These approaches have resulted in the detection of several specific autoantibodies, alterations of CD95/Fas and its related molecules, and evidence of chronic activation of responder T cells and regulatory T cells following silica exposure. In this review, we present details of our investigations as an introduction to scientific approaches examining the immunological effects of environmental and occupational substances.
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    ABSTRACT: Caplan originally described distinctive pulmonary nodules in miners who had suffered from rheumatoid arthritis. Later, the pulmonary nodules, together with a history of rheumatoid arthritis and exposure to inorganic dust were called Caplan's syndrome. This syndrome has been de-scribed by case reports in many countries but only two cases have been reported in Korea up to now. The patient in this case report was a 70-years-old man who had worked in the construction field for 20 years mainly de-molishing buildings. He was diagnosed with silicosis by a lung biopsy 1 year prior to admission. He suddenly devel-oped arthralgia and morning stiffness in multiple joints 2 weeks prior to admission. Chest imaging revealed ag-gravation of the bilateral pulmonary nodules. He was diag-nosed with seropositive rheumatoid arthritis. The lung nodules, arthralgia, and morning stiffness improved clin-ically after treatment with the corticosteroid and disease modifying anti-rheumatic drugs.
    Journal of Rheumatic Diseases. 01/2011; 18(1).

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