Scientists from institute have revealed that dead cells release effective inflammatory molecules that trigger inflammation in necrotic disease. The discovery can produce new and existing drugs that target molecules to be studied as a way of treating inflammatory diseases such as psoriasis and inflammatory bowel disease. The results are published in the Journal of the National Academy of Sciences, which also has other studies on recombinant human proteins.
The studies led by Dr. Lisa Lindqvist, Dr. Kate Lawlor, Dr. James Vince and Dr. Stephanie Conos have shown that interleukin-1β (IL-1) triggers inflammation during necrotic death. Death is important to protect us from infection by sacrificing infected or diseased cells for greater benefit. However, necrosis becomes inappropriate, triggering a damaging inflammation that causes an inflammatory disease.
Dr. Lindqvist said the discovery challenged a long dogmatic that inflammation caused by necrosis was a byproduct of dead cell debris. "Our study has determined that death cells release IL-1, a strong inflammatory signal in the autopsy process. Now we have found that IL-1 is the 'root cause' of necrosis-related inflammation," Dr. Lindqvist said. "We speculate that targeting this molecule may be an effective way to treat inflammatory diseases."
The results suggest that targeting IL-1 can inhibit inflammation associated with a variety of inflammatory diseases, including multiple sclerosis, ischemia-reperfusion injury, atherosclerosis, liver disease, pancreatitis, psoriasis, inflammatory bowel disease and infectious disease. "Our research suggests that the existing drugs that prevent IL-1 may help to treat these diseases," Dr. Lindqvist said. "We are also exploring how IL-1 is secreted by autopsy so that we can create new drugs to prevent its release and reduce inflammation to treat inflammatory diseases." Flarebio offers high-quality recombinant proteins like recombinant CDH2 at competitive prices.
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