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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 3 372 6788

Research interests

Professor Madhav Bhatia's research focuses on inflammation, and he is the head of the Inflammation Research Group at the University of Otago, Christchurch.

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

His research has shown hydrogen sulfide and substance P as mediators of inflammation and potential therapeutic targets for inflammatory diseases. Professor Bhatia is interested in defining the mechanism by which hydrogen sulfide and substance P contribute to inflammation.

The Group's research has shown a key role of chemokines in inflammatory diseases, and of pancreatic acinar cell apoptosis in acute pancreatitis. The Group has also been working on novel markers for diagnosis and prognosis of inflammatory and infectious diseases

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

Publications to peer reviewed literature: More than 190 papers and review articles, and more than 130 abstracts published in journals.

Citations: More than 14000 (One article cited more than 1000 times, and 39 articles cited more than 100 times).

“h” index: 60

  1. Zhu Z, Chambers S, Zeng Y, and Bhatia M. Gases in sepsis: novel mediators and therapeutic targets. Int J Mol Sci. 2022; 23: 3669.
  2. Lian X, Scott-Thomas A, Lewis JG, Bhatia M, MacPherson S, Zeng Y, and Chambers S. Monoclonal antibody and invasive aspergillosis: diagnostic and therapeutic perspectives. Int J Mol Sci. 2022; 23: 5563.
  3. Kumar A, and Bhatia M. Role of hydrogen sulfide, substance P, and adhesion molecules in acute pancreatitis. Int J Mol Sci. 2021; 22: 12136.
  4. Patel BK, Patel KH, Bhatia M, Iyer SG, Madhavan KK, and Moochhala SM. Gut microbiome in acute pancreatitis-A review based on current literature. World J Gastroenterol. 2021; 27: 5019-5036.
  5. Bhatia M, and Gaddam R. Hydrogen sulfide in inflammation: a novel mediator and therapeutic target. Antioxid Redox Signal. 2021; 34: 1368-1377.
  6. Dawoodbhoy FM, Patel BK, Patel K, Bhatia M, Lee CN, and Moochhala SM. Gut microbiota dysbiosis as a target for improved post-surgical outcomes and improved patient care. A review of current literature. Shock. 2021; 55: 441–454.
  7. Bhatia M. Understanding hydrogen sulfide in inflammation: opportunities and challenges (Editorial). Mol Cell Ther. 2019; 7: 9-14.
  8. Gaddam RR, Jha P, and Bhatia M. The infections and hydrogen sulfide. Frontiers in Anti-Infective Drug Discovery. (Eds. Rahman AU, and Choudhary MI). 2018; 7: 261-272.
  9. 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.
  10. 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.
  11. Bhatia M. H2S and inflammation - an overview. Handb Exp Pharmacol. 2015; 230: 165-180.
  12. Bhatia M. H2S and substance P in inflammation. Meth Enzymol. 2015; 555: 195-205.
  13. 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.
  14. Rivers J, Badiei A, and Bhatia M. Hydrogen sulfide as a therapeutic target for inflammation. Expert Opin Ther Targets. 2012; 16: 439-449.
  15. Bhatia M. Hydrogen sulfide and substance P in inflammation. Antioxid Redox Signal. 2010; 12: 1191-1202.

Inaugural Professorial Lectures

Madhav Bhatia delivers his Inaugral Professorial Lecture
Watch Prof. Bhatia's IPL, Inflammation: A new frontier of medicine, Feb 2011.
Part 1, Part 2, Part 3

Publications

Shahid, A., & Bhatia, M. (2024). Hydrogen sulfide: A versatile molecule and therapeutic target in health and diseases. Biomolecules, 14, 1145. doi: 10.3390/biom14091145 Journal - Research Other

Zhu, Z., Chambers, S., & Bhatia, M. (2024). Substance P promotes leukocyte infiltration in the liver and lungs of mice with sepsis: A key role for adhesion molecules on vascular endothelial cells. International Journal of Molecular Sciences, 25(12), 6500. doi: 10.3390/ijms25126500 Journal - Research Article

Zhu, Z., Chambers, S., & Bhatia, M. (2024). Suppressing the substance P-NK1R signalling protects mice against sepsis-associated acute inflammatory injury and ferroptosis in the liver and lungs. Antioxidants, 13, 300. doi: 10.3390/antiox13030300 Journal - Research Article

Manandhar, S., Gaddam, R. R., Chambers, S., & Bhatia, M. (2024). Kupffer cell inactivation alters endothelial cell adhesion molecules in cecal ligation and puncture-induced sepsis. Biomolecules, 14, 84. doi: 10.3390/biom14010084 Journal - Research Article

Relja, B., Ghezzi, P., Coldewey, S. M., Pavlov, V. A., Bhatia, M., Jungwirth, B., & Thiemermann, C. (2024). Community series in translational insights into mechanisms and therapy of organ dysfunction in sepsis and trauma: Volume III. Frontiers in Immunology, 15, 1447892. doi: 10.3389/fimmu.2024.1447892 Journal - Research Other

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