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• W2465432486 abstract "Silica exposure has been associated with formation of autoantibodies and development o f several autoimmune diseases, however, mechanisms leading to these events are unknown. Therefore, the effect o f silica on autoimmune disease progression in autoimmune-prone New Zealand mixed mice was studied. Following silica exposure, NZM mice developed high levels o f proteinuria and died prematurely due to immune complex and complement deposition within the glomerulus o f the kidney as compared to saline and TiOa exposed mice. Further, silica exposure resulted in higher levels of autoantibodies to nuclear antigen, specifically histones, than saline or TiOa exposed mice. These effects were mediated in part by the migration of high numbers o f CD4+ T cells and B la B cells to local lymph nodes as well as the decrease in the number of CD4+CD25+ regulatory T cells. Silica exposure induced a shift in the Thl/Th2 balance in favor o f a Thl response as measured by alterations in immunoglobulin isotypes. The increase in autoantibodies following silica exposure in NZM mice involved autoantibodies which preferentially recognized apoptotie cells. Following silica exposure, alveolar macrophages from NZM mice were shown to have increased gene expression levels of several apoptosis genes. Most prominent was an increase in proapoptotic protein kinase C6 in alveolar macrophages from silica exposed NZM mice. Using an in vitro model, PKC6 was found to mediate apoptosis in silica treated bone marrow derived macrophages. Further, TNF-a was found to be chronically elevated in lung lavage fluid possibly adding to the induction of apoptosis. Inhibiting the apoptotie response induced by silica in alveolar macrophages using an inhibitor o f PKC6 in vivo significantly reduced silica exacerbated systemic autoimmune disease. Inhibition of PKC5 in vivo resulted in decreased proteinuria, kidney disease and anti-histone autoantibodies. These results suggest that silica exposure resulted in apoptosis o f alveolar macrophages and by blocking apoptosis through PKC6 the exacerbation o f systemic autoimmune disease in NZM mice was inhibited. These data taken together may provide insights into mechanisms by which xenobiotics induce apoptosis and the role apoptosis may play in the progression of systemic autoimmune disease." @default.
• W2465432486 created "2016-07-22" @default.
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• W2465432486 date "2004-01-01" @default.
• W2465432486 modified "2023-09-24" @default.
• W2465432486 title "Mechanisms of silica exacerbated systemic autoimmune disease in New Zealand mixed mice" @default.
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