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Inflammation The apoptotic cascade and the attendant mechanisms that trigger inflammation are a complex network of receptors, transcription factors and potent cytokines. Under certain circumstances cytokine-induced cell death can contribute to the pathology of inflammatory conditions, including type-1 diabetes. Senesco has shown that small inhibitory RNAs (siRNAs) that modulate eIF5A expression have the ability to downregulate the NF-kB pathway and the production of inflammatory cytokines. We have demonstrated that the siRNA can protect cells from premature death in models of diabetes and lung inflammation. Consequently we believe that our technology could be applicable to certain inflammatory diseases. When eIF5A siRNA was delivered intransally to mice that had been treated with LPS, TNFa and IL1a levels were both reduced by more than 95% in the lungs. In another LPS challenge experiment eIF5A siRNA pre-treated mice had significantly reduced blood levels of multiple pro-inflammatory cytokines, including TNFa and interleukins 1, 2, 6, 12, MIP-1a, and IFN-g. Importantly cytokine IL10, a down-regulator of pro-inflammatory cytokines, was unaffected. A significant increase in the survival of insulin-producing pancreatic islet cells was achieved when mice received eIF5A1 siRNA. Concurrently, it was shown that the death of islet cells, resulting from exposure to IL-1b and IFN-g, was significantly reduced. If you have more technical questions or interests, please contact us directly at info@senesco.com. Back to Top |
