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Madhav BhatiaGroup Leader, Inflammation Research Group
Co-ordinator, BBiomedSc(Hons) Programme

BSc(Hons), MSc, PhD (All India Institute of Medical Sciences)

Email madhav.bhatia@otago.ac.nz 
Tel 64 3 378 6238

Research interests

Professor Madhav Bhatia’s research focuses on inflammation. He leads an active research programme on the molecular pharmacology and molecular pathology of inflammatory conditions, such as acute pancreatitis, polymicrobial sepsis, burns, and arthritis.

Professor Bhatia’s research has shown hydrogen sulfide and substance P as mediators of inflammation and potential therapeutic targets for inflammatory diseases. He is interested in defining the mechanism by which hydrogen sulfide and substance P contribute to inflammation. His research has also shown a key role of chemokines in inflammatory diseases, and of pancreatic acinar cell apoptosis in acute pancreatitis.

The long term goal of this research is to translate this knowledge to the clinic, and early results in this direction have been promising.

Funding

The Inflammation Research Group is supported by:

  • Lottery Health
  • Canterbury Medical Research Foundation
  • Arthritis New Zealand
  • University of Otago Research Grant
  • Maurice & Phyllis Paykel Trust 
  • Health Reseach Council of New Zealand Singapore Networking Grant
  • Royal Scoiety of New Zealand's Catalyst: Leaders New Zealand-China Scientist Exchange Programme

Prior to moving to Christchurch, Professor Bhatia's research was supported by research grants from Biomedical Research Council, Singapore, National Medical Research Council, Singapore, Academic Research Fund, National University of Singapore, Singapore, and Defence Science and Technology Agency-National University of Singapore Joint Applied R&D Co-operation Programme, Singapore.

Major review articles

  1. Pan LL, Li J, Shamoon M, Bhatia M, and Sun J. Recent advances on nutrition in treatment of acute pancreatitis. Front Immunol. 2017; 8: 762.
  2. Shamoon M, Chen Y, Bhatia M, and Sun J. Therapeutic implications of innate immune system in acute pancreatitis. Expert Opin Ther Targets. 2016; 20: 73-87.
  3. Bhatia M. H2S and inflammation - an overview. Handb Exp Pharmacol. 2015; 230: 165-180.
  4. Bhatia M. H2S and substance P in inflammation. Meth Enzymol. 2015; 555: 195-205.
  5. Bhatia M, Zemans RL, and Jeyaseelan S. Role of chemokines in the pathogenesis of acute lung injury. Amer J Resp Cell Mol Biol. 2012; 46: 566-572.
  6. Rivers J, Badiei A, and Bhatia M. Hydrogen sulfide as a therapeutic target for inflammation. Expert Opin Ther Targets. 2012; 16: 439-449.
  7. Bhatia M. Hydrogen sulfide and substance P in inflammation. Antioxid Redox Signal. 2010; 12: 1191-1202.
  8. Bhatia M, Wong FL, Cao Y, Lau HY, Huang J, Puneet P, and Chevali L. Pathophysiology of acute pancreatitis. Pancreatology. 2005; 5:132-144.
  9. Bhatia M. Hydrogen sulfide as a vasodilator. IUBMB Life. 2005; 57: 603-606.
  10. Puneet, P, Moochhala, S, and Bhatia, M. Chemokines in acute respiratory distress syndrome. Am J Physiol Lung Cell Mol Physiol. 2005; 288: L3-L15.
  11. Bhatia M. Inflammatory response on the pancreatic acinar cell injury. Scand J Surg. 2005; 94: 97-102.
  12. Bhatia M, and Moochhala S. Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome. J Path. 2004; 202: 145-156.
  13. Bhatia M. Apoptosis versus necrosis in acute pancreatitis. Am J Physiol Gastrointest Liver Physiol. 2004; 286: G189-196.
  14. Moore PK, Bhatia M, and Moochhala, S. Hydrogen sulphide: from the smell of the past to the mediator of the future? Trends Pharmacol Sci. 2003; 24: 609-611.
  15. Bhatia M, Brady M, Shokuhi S, Christmas SE, Neoptolemos JP, and Slavin J. Inflammatory mediators in acute pancreatitis. J Pathol. 2000; 190: 117-125.