ABSTRACT
This review is partly composed of the presentation "Cytokine alteration and speculated immunological pathophysiology in silicosis and asbestos-related diseases" delivered during the symposium "Biological effects of fibrous and particulate substances and related areas" organized by the Study Group of Fibrous and Particulate Studies of the Japanese Society of Hygiene and held at the 78th Annual Meeting in Kumamoto, Japan. In this review, we briefly introduce the results of recent immunological analysis using the plasma of silica and asbestos-exposed patients diagnosed with silicosis, pleural plaque, or malignant mesothelioma. Thereafter, experimental background and speculation concerning the immunological pathophysiology of silica and asbestos-exposed patients are discussed.
ABSTRACT
<p><b>OBJECTIVES</b>The aim of this study was to detect anti-topoisomerase I (anti-topo I) autoantibodies, which are known to be limited in systemic sclerosis patients, in silicosis patients with no clinical symptoms of autoimmune disease.</p><p><b>METHODS</b>Serum anti-topo I autoantibodies were detected using ELISA. Differences in clinical parameters between patients with and without anti-topo I autoantibodies were analyzed.</p><p><b>RESULTS</b>Seven of 69 patients had anti-topo I autoantibodies. These 7 patients showed elevated PaCO(2) values (P=0.0212), and inverse correlations between serum soluble Fas levels and PaCO(2) values were found.</p><p><b>CONCLUSION</b>Anti-topo I autoantibodies were detected in 10.1% of silicosis patients without any clinical symptoms of autoimmune disease. The findings here suggest that the genesis of anti-topo I autoantibodies might be related to pulmonary involvement or lung fibrosis associated with progression of silicosis.</p>
ABSTRACT
Objectives: The aim of this study was to detect anti-topoisomerase l (anti-topo I) autoantibodies, which are known to be limited in systemic sclerosis patients, in silicosis patients with no clinical symptoms of autoimmune disease. Methods: Serum anti-topo I autoantibodies were detected using ELISA. Differences in clinical parameters between patients with and without anti-topo I autoantibodies were analyzed. Results: Seven of 69 patients had anti-topo I autoantibodies. These 7 patients showed elevated PaCO2 values (P=0.0212), and inverse correlations between serum soluble Fas levels and PaCO2 values were found. Conclusion: Anti-topo I autoantibodies were detected in 10.1% of silicosis patients without any clinical symptoms of autoimmune disease. The findings here suggest that the genesis of anti-topo l autoantibodies might be related to pulmonary involvement or lung fibrosis associated with progression of silicosis.