Inflammation Research Group
Professor Madhav Bhatia, who joined the Department in Jan 2010 from the National University of Singapore, heads the Inflammation Research Group.
The group has an active research programme on the molecular pharmacology and molecular pathology of various inflammatory conditions such as acute pancreatitis, polymicrobial sepsis and burns with the long-term goal of developing clinically effective therapeutic approaches.
Current areas of interest
Gas Mediators in Inflammation
Hydrogen sulfide (H2S) is a toxic gas and an environmental pollutant. H2S is responsible for the “rotten egg” odour of spring waters in the Rotorua district.
H2S is also produced in the body and acts as a biological mediator. We are currently looking at the role of H2S in inflammation, particularly in conditions such as acute pancreatitis, septic shock, and burns. We have shown, for the first time, a role of endogenously produced H2S as a mediator of inflammation in these disease conditions. Studies are on to investigate the mechanism by which H2S acts as a mediator of inflammation.
Neurogenic Inflammation in Acute Pancreatitis, Sepsis, and Burns
Substance P is a neuropeptide that acts via neurokinin-1 (NK1) receptors and plays an important role in many of the inflammatory states.
The current research aims to investigate the pro-inflammatory role of substance P and other neuroinflammatory mediators in acute pancreatitis, sepsis, and burns. For this purpose, we are using experimental models of disease.
Chemokines in Acute Pancreatitis, Sepsis, and Burns
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 role of chemokines in acute pancreatitis, sepsis and burns.
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. Little is known, though, about the mechanism of apoptosis in the pancreatic acinar cell.
Research in the laboratory aims to investigate the molecular mechanism of pancreatic acinar cell apoptosis and its role in acute pancreatitis.
Postgraduate study opportunities
We are looking for enthusiastic and motivated students to do their postgraduate study with the Inflammation Research Group.
Scholarship funding is available to eligible students to undertake their PhD with us. We also offer a one year Honours Degree.