Virus infection-induced NLRP3 inflammasomes generate hyper-immune responses and inflammation by various interleukins and cytokines and infiltration of other immune cells (mainly fibroblasts, macrophages, and alveolar epithelial cells (AECs)) in the formation and development of pulmonary fibrosis by regulating inflammation, immune response, autophagy, senescence, EMT, potentially leading to pulmonary fibrosis [110,111]. This evidence concerns the gene NLRP3 and pulmonary fibrosis.