First, our data show that HFD+CKD (UTs) promote extracellular LPS enter aortic cell cytosol, increase intracellular gram-negative bacterial infections in CKD (79, 80), increase intracellular crystallization of CKD-elevated PA, activate CASP4/11 and N-GSDMD membrane expression, increase secretion of IL1B and other CASP11-GSDMD secretome, and upregulate TI genes in aortic cells. This evidence concerns the gene IL1B and chronic kidney disease.