Journal
MEDIATORS OF INFLAMMATION
Volume 2016, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2016/6235614
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Funding
- National Natural Science Foundation of China [81273045]
- Program for Liaoning Innovative Research Team in University [LT2015028]
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CD4(+) T cells play an important role in regulating silica-induced inflammation and fibrosis. Recent studies showed that Wnt/beta-catenin pathway could modulate the function and the differentiation of CD4(+) T cells. Therefore, Wnt/beta-catenin pathway may participate in the development and progress of silicosis. To investigate the role of Wnt/beta-catenin pathway, we used lentivirus expressing beta-catenin shRNA to block the Wnt/beta-catenin pathway by intratracheal instillation to the mice model of silicosis. Treatment of lentivirus could significantly aggravate the silica-induced lung inflammation and attenuated the fibrosis at the late stage. By analyzing CD4(+) T cells, we found that blockade of Wnt/beta-catenin pathway suppressed regulatory T cells (Tregs). Reciprocally, enhanced Th17 response was responsible for the further accumulation of neutrophils and production of proinflammatory cytokines. In addition, blockade of Wnt/beta-catenin pathway delayed the Th1/Th2 polarization by inhibiting Tregs and Th2 response. These results indicated that Wnt/beta-catenin pathway could regulate Tregs to modulate Th immune response, which finally altered the pathological character of silicosis. Our study suggested that Wnt/beta-catenin pathway might be a potential target to treat the silica-induced inflammation and fibrosis.
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