The research focus of the Inflammation Research Group is to investigate the role of inflammatory mediators in the pathogenesis of different inflammatory conditions, such as acute pancreatitis, septic shock, burns, and arthritis, with the long-term goal of developing clinically effective therapeutic approaches. We have also been working on novel markers for diagnosis and prognosis of inflammatory and infectious diseases. Current areas of interest include:
Hydrogen sulfide in inflammation
Hydrogen sulfide is a toxic gas and an environmental pollutant. It is responsible for the “rotten egg” odour of spring waters in the Rotorua district area. Hydrogen sulfide is also produced in the body and acts as a biological mediator. We are currently looking at the role of hydrogen sulfide in inflammation. We have shown, for the first time, a role of endogenously produced hydrogen sulfide as a mediator of inflammation in acute pancreatitis, septic shock, burns, and arthritis (rheumatoid arthritis and gout). Studies are on to investigate the mechanism by which hydrogen sulfide acts as a mediator of inflammation.
Substance P in inflammation
Substance P is a neuropeptide that acts via neurokinin-1 receptors and plays an important role in many of the inflammatory states. We have shown a key role of substance P in inflammation in acute pancreatitis, sepsis, and burn injuries. The current research aims to investigate the role of substance P in inflammatory disease, and the mechanism by which it acts in inflammation.
Chemokines in inflammation
The systemic effects of acute pancreatitis have many similarities to those of sepsis and burns. The haemodynamic features of cardiovascular instability, reduced ejection fraction and decreased systemic vascular resistance are indistinguishable in each of these conditions. Chemokines play a critical role in the pathogenesis of all these conditions. Chemokines influence leukocyte migration into tissues and regulate leukocyte activation in situ. Studies are in progress to investigate the mechanism by which chemokines contribute to inflammatory disease.
Apoptosis of pancreatic acinar cells
Apoptosis, or programmed cell death, is an energy consuming, genetically regulated form of cell death with little or no inflammatory reaction. We have shown that administration of crambene (1-cyano-2-hydroxy-3-butene - CHB), a plant nitrile, induces extensive acinar cell apoptosis in the pancreas, and protects against inflammation in acute pancreatitis. Research in the laboratory aims to investigate the molecular mechanism of pancreatic acinar cell apoptosis and the mechanism by which this apoptosis protects against acute pancreatitis.