LPS bind to TLR4, induce GBPs expression, and mediate caspase-11 pathway to participate in renal tubulointerstitial inflammation. LPS combined with TLR4, activate the NF-kB signaling pathways. They enhance NLRP3 expression in renal epithelial cells, and participate in the kidney inflammation and fibrosis. This evidence concerns the gene NFKB1 and inflammatory response.