NLRP3 participates in the regulation of EMT in bleomycin-induced pulmonary fibrosis

- EMT participated in the process of BLM-induced pulmonary fibrosis.
- The NLRP3 inflammasome was activated in the type II alveolar epithelial cells.
- The NLRP3 may modulate EMT through TGF-β1 signaling pathway.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and irreversible lung disease. Studies have shown that epithelial-mesenchymal transition (EMT) plays an important role in the development of IPF. The NLRP3 inflammasome is reported to be activated and play an important role in many respiratory diseases. However, whether the NLRP3 inflammasome is activated in alveolar epithelial cells as well as the regulatory role of NLRP3 in EMT have not been reported. In this study, we transfected NLRP3 siRNA into A549 and RLE-6TN cells and treated them with bleomycin (BLM) for 24 h. Then, we detected the expression of NLRP3 inflammasome-related proteins, EMT-related proteins and transforming growth factor-β1 (TGF-β1) via western blotting, immunofluorescence and real-time quantitative PCR. The mRNA and protein level of NLRP3, ASC and caspase-1 increased after treatment with BLM. The IL-1β levels were significantly decreased after inhibition of NLRP3 and caspase-1. E-cadherin expression increased and α-SMA was reduced in the BLM group when inhibited by NLRP3. The level of TGF-β1 was reduced after NLRP3 silencing. These results indicated that the NLRP3 inflammasome was activated in alveolar epithelial cells and that NLRP3 may regulate EMT through TGF-β1. These results may extend our understanding of the mechanism of pulmonary fibrosis and provide a new therapeutic target for pulmonary fibrosis.

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