Other studies however, did not observe increased baseline apoptosis in respiratory epithelial cells expressing mutant CFTR except after exposure of the cells to P. aeruginosa. In contrast, several other studies reported that expression of defective CFTR or knockdown of CFTR protects against apoptosis phenotype. CF knockout mice exhibited a baseline proinflammatory state and an anti-apoptotic phenotype in the pancreas and showed failed induction of apoptosis in response to P. aeruginosa. Recently, delayed apoptosis has been described in polymorphonuclear neutrophil from CF patients, which might explain PMN persistence in the CF lung. Our study showed increased baseline apoptosis in AM with CFTR knockdown. The increased apoptosis of inflammatory cells such as macrophages and neutrophils has been Veratramine considered as an anti-inflammatory phenotype, however our study showed both augmented apoptosis and increased proinflammatory in AM with CFTR knockdown. Altered apoptosis has not been described for disruption of other epithelial chloride channels, including members of volume-regulated chloride channel CLC family. We suggested that as a consequence of more proinflammatory cytokine Colistin Sulfate production the cells are prone to undergo apoptosis. Consistent with our findings, increased Cav1 has been observed in murine peritoneal macrophages undergoing apoptosis. These contradictory observations could be related to cell type-specific responses and/or the agents used to induce apoptosis. Again, as outlined above, the phenotype of AM in the CF lung may not be accurately predicted by the short term culture results of our study. Defective or absent CFTR is known to be associated with abnormalities in the cellular lipid metabolism. The mSREBP and membrane free cholesterol levels have been shown to be increased in epithelial cells that express defective CFTR. It is, however not clear whether these changes in cholesterol metabolism are cell-type or CFTR mutation specific, i.e. only found in cells that express DF508 CFTR protein. Notably, knockdown of CFTR in human AM did not affect total and free cellular cholesterol levels in our study.