Professor Damian Mole
Our ultimate aim is to improve the outcome of patients with severe acute pancreatitis by understanding the mechanisms and developing novel therapies which protect against multiple organ dysfunction.
- Jim Black - Technician
- Jay Kulkarni - Clinical Research PhD Fellow
- Kris McGuire – Postdoc
- Lucile Neyton - MRC Presicion Medicine PhD student
- James O'Kelly - Clinical Research PhD Fellow
- Sandra Spratt - Technician
- Heather Waddell - MRC Precision Medicine PhD student
- Kate Walker - Technician
- Xiaozhong Zheng - Research Fellow (email)
Acute pancreatitis is a common and devastating disease. Inflammation in the pancreas is triggered usually by gallstones or excessive alcohol consumption. Most patients have a self-limiting form of disease, but approximately 20% develop organ failure of other organs, notably the lungs, kidneys and cardiovascular system, which means these patients need intensive care or high-dependency unit support. At present the mortality of those needing ICU to help treat acute pancreatitis is 20%. Approximately 4% of all ICU bed days are taken up with severe acute pancreatitis or its complications. There is no specific therapy to help these patients.
We have identified that the kynurenine pathway of tryptophan is an important contributor to the many inflammatory mechanisms that play a role in severe acute pancreatitis. By using experimental models in cells and in rats and mice with experimental acute pancreatitis, we have advanced our understanding of how this pathway is involved in pancreatitis and are in a position to develop new medicines to take to clinical application in patients.