Our in vivo data and the lack of IL-1b in glomerular isolates raise doubts about the functional role of the NLRP3 inflammasomemediated caspase-1 activation in glomerular cells. We therefore examined whether mesangial cells, glomerular endothelial cells , podocytes, and renal dendritic cells are able to mount IL- 1b release. All glomerular cells highly express TLR2 and TLR4. We prestimulated each of these cell types with TLR4 agonist LPS or TLR2 agonist Pam3CSK4 and challenged them with the NLRP3 agonist ATP as done with isolated intact glomeruli. First, we quantified IL-1b secretion by ELISA in supernatants 24 hours after stimulation. Among all cell types tested only renal dendritic cells induced IL-1b purchase Epoxomicin release . Pro-IL-1b protein expression, the mature IL-1b form, and caspase-1 activation were assessed by Western blot after 6 hours of stimulation as before. Consistent with the results from glomerular isolates LPS did not induce pro-IL-1b protein, IL-1b maturation or caspase-1 activation in glomerular cells . Obviously, TLR4 activation does neither induce pro-IL-1b as the necessary first step for inflammasome�Cmediated IL-1b release nor did it activate caspase-1 in mesangial cells, GEnC, and podocytes. However, renal dendritic cells shared the capacity of caspase-1 activation and IL-1b secretion with BMDCs . We therefore conclude that inside the kidney immune cells like CD11c+ DCs are capable of secreting active IL-1b upon inflammasome activation but this function is not shared by intrinsic glomerular cells due to an inability to induce pro-IL-1b upon TLR4 activation or to activate caspase-1 upon ATP exposure. Previously published tubulointerstitial gene PF-4217903 expression data from patients with diabetic nephropathy , focal-segmental glomerulosclerosis , IgA nephropathy , and membranous glomerulonephritis were compared to data of nonprogressive proteinuric states such as minimal change disease , and healthy controls . Consistent with the finding that progressive proteinuric diseases are associated with tubulointerstitial inflammation, most of the IL- 1 and inflammasome related genes were significantly regulated in progressive diseases, whereas transcript levels were unchanged in MCD compared with controls . As CASP1 showed an induction in all progressive diseases, we further dissected its expression in glomerular and tubulointerstitial samples of patients with different progressive glomerulopathies by real-time RT-PCR. Only in the tubulointerstitial cThe NLRP3 inflammasome-mediated activation of caspase-1 contributes to a large spectrum of inflammatory diseases but so far little is known about its role in renal inflammation .