S100A4 Promotes BCG-Induced Pyroptosis of Macrophages by Activating the NF-κB/NLRP3 Inflammasome Signaling Pathway

Pyroptosis is a host immune strategy to defend against Mycobacterium tuberculosis (Mtb) infection. S100A4, calcium-binding protein that plays an important role in promoting cancer progression as well the pathophysiological development of various non-tumor diseases, has not been explored Mtb-infected hosts. In this study, transcriptome analysis peripheral blood patients with pulmonary (PTB) revealed S100A4 and GSDMD were significantly up-regulated PTB patients’ blood. Furthermore, there was positive correlation between expression S100A4. KEGG pathway enrichment showed differentially expressed genes healthy controls related inflammation, such NOD-like receptor signaling NF-κB pathway. To investigate regulatory effects on macrophage pyroptosis, THP-1 macrophages infected Bacillus Calmette-Guérin (BCG) pre-treated exogenous inhibitor or si-S100A4. This research study shown promotes pyroptosis caused by BCG infection activates NLRP3 inflammasome pathways, which can be inhibited knockdown inhibition addition, blocks promotion effect BCG-induced macrophages. conclusion, NF-κB/NLRP3 promote induced Mtb These data provide new insights into how affects Mtb-induced pyroptosis.