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Health Sciences profile

Professor Madhav Bhatia

PositionProfessor
DepartmentDepartment of Pathology (UOC)
QualificationsBSc(Hons), MSc, PhD
Research summaryInflammation

Research

I am the Leader of the Inflammation Research Group. My current research focuses on inflammation. The research strengths that I have brought to the University of Otago are experimental models of inflammation. These models of diseases were missing at the University, even though these diseases are major health problems in New Zealand and worldwide. My group uses these models to investigate disease mechanisms and develop novel therapeutic approaches. The long term goal of this research is to translate this knowledge to the clinic, and early results in this direction have been promising.

Research in my group is supported by research grants from Lottery Health, University of Otago Research Grant, and Health Reseach Council of New Zealand Singapore Networking Grant.

Publications

Muniraj, N., Stamp, L. K., Badiei, A., Hegde, A., Cameron, V., & Bhatia, M. (2017). Hydrogen sulfide acts as a pro-inflammatory mediator in rheumatic disease. International Journal of Rheumatic Diseases, 20(2), 182-189. doi: 10.1111/1756-185x.12472

Ang, A. D., Rivers-Auty, J., Hegde, A., Ishii, I., & Bhatia, M. (2013). The effect of CSE gene deletion in caerulein-induced acute pancreatitis in the mouse. American Journal of Physiology: Gastrointestinal & Liver Physiology, 305, G712-G721. doi: 10.1152/ajpgi.00044.2013

Badiei, A., Rivers-Auty, J., Ang, A. D., & Bhatia, M. (2013). Inhibition of hydrogen sulfide production by gene silencing attenuates inflammatory activity of LPS-activated RAW264.7 cells. Applied Microbiology & Biotechnology, 97(17), 7845-7852. doi: 10.1007/s00253-013-5080-x

Ang, S.-F., Moochhala, S. M., MacAry, P. A., & Bhatia, M. (2011). Hydrogen sulfide and neurogenic inflammation in polymicrobial sepsis: Involvement of substance P and ERK-NF-κB signaling. PLoS ONE, 6(9), e24535. doi: 10.1371/journal.pone.0024535

Sio, S. W. S., Moochhala, S., Lu, J., & Bhatia, M. (2010). Early protection from burn-induced acute lung injury by deletion of preprotachykinin-A gene. American Journal of Respiratory & Critical Care Medicine, 181(1), 36-46. doi: 10.1164/rccm.200907-1073OC

Journal - Research Article

Muniraj, N., Stamp, L. K., Badiei, A., Hegde, A., Cameron, V., & Bhatia, M. (2017). Hydrogen sulfide acts as a pro-inflammatory mediator in rheumatic disease. International Journal of Rheumatic Diseases, 20(2), 182-189. doi: 10.1111/1756-185x.12472

Badiei, A., Rivers-Auty, J., Ang, A. D., & Bhatia, M. (2013). Inhibition of hydrogen sulfide production by gene silencing attenuates inflammatory activity of LPS-activated RAW264.7 cells. Applied Microbiology & Biotechnology, 97(17), 7845-7852. doi: 10.1007/s00253-013-5080-x

Ang, A. D., Rivers-Auty, J., Hegde, A., Ishii, I., & Bhatia, M. (2013). The effect of CSE gene deletion in caerulein-induced acute pancreatitis in the mouse. American Journal of Physiology: Gastrointestinal & Liver Physiology, 305, G712-G721. doi: 10.1152/ajpgi.00044.2013

Bhatia, M., Zemans, R. L., & Jeyaseelan, S. (2012). Role of chemokines in the pathogenesis of acute lung injury. American Journal of Respiratory Cell & Molecular Biology, 46(5), 566-572. doi: 10.1165/rcmb.2011-0392TR

Sidhapuriwala, J. N., Hegde, A., Ang, A. D., Zhu, Y. Z., & Bhatia, M. (2012). Effects of S-Propargyl-Cysteine (SPRC) in caerulein-induced acute pancreatitis in mice. PLoS ONE, 7(3), e32574. doi: 10.1371/journal.pone.0032574

Ang, A. D., Konigstorfer, A., Giles, G. I., & Bhatia, M. (2012). Measuring free tissue sulfide. Advances in Biological Chemistry, 2(4), 360-365. doi: 10.4236/abc.2012.24044

Koh, Y.-H., Tamizhselvi, R., Moochhala, S., Bian, J.-S., & Bhatia, M. (2011). Role of protein kinase C in caerulein induced expression of substance P and neurokinin-1-receptors in murine pancreatic acinar cells. Journal of Cellular & Molecular Medicine, 15(10), 2139-2149. doi: 10.1111/j.1582-4934.2010.01205.x

Ang, S.-F., Moochhala, S. M., MacAry, P. A., & Bhatia, M. (2011). Hydrogen sulfide and neurogenic inflammation in polymicrobial sepsis: Involvement of substance P and ERK-NF-κB signaling. PLoS ONE, 6(9), e24535. doi: 10.1371/journal.pone.0024535

Ang, S.-F., Sio, S. W. S., Moochhala, S. M., MacAry, P. A., & Bhatia, M. (2011). Hydrogen sulfide upregulates cyclooxygenase-2 and prostaglandin E metabolite in sepsis-evoked acute lung injury via transient receptor potential vanilloid type 1 channel activation. Journal of Immunology, 187(9), 4778-4787. doi: 10.4049/jimmunol.1101559

Koh, Y.-H., Moochhala, S., & Bhatia, M. (2011). The role of neutral endopeptidase in caerulein-induced acute pancreatitis. Journal of Immunology, 187, 5429-5439. doi: 10.4049/jimmunol.1102011

Sio, S. W. S., Moochhala, S., Lu, J., & Bhatia, M. (2010). Early protection from burn-induced acute lung injury by deletion of preprotachykinin-A gene. American Journal of Respiratory & Critical Care Medicine, 181(1), 36-46. doi: 10.1164/rccm.200907-1073OC

Ang, S.-F., Moochhala, S. M., & Bhatia, M. (2010). Hydrogen sulfide promotes transient receptor potential vanilloid 1-mediated neurogenic inflammation in polymicrobial sepsis. Critical Care Medicine, 38(2), 619-628. doi: 10.1097/CCM.0b013e3181c0df00

Ramnath, R. D., Sun, J., & Bhatia, M. (2010). PKC δ mediates pro-inflammatory responses in a mouse model of caerulein-induced acute pancreatitis. Journal of Molecular Medicine, 88, 1055-1063. doi: 10.1007/s00109-010-0647-9

Hegde, A., Uttamchandani, M., Bhatia, M., & Moochhala, S. M. (2010). Plasma cytokine profiles in Preprotachykinin-A knockout mice subjected to polymicrobial sepsis. Molecular Medicine, 16(1-2), 45-52. doi: 10.2119/molmed.2009.00112

Bhatia, M. (2010). Hydrogen sulfide and substance P in inflammation. Antioxidants & Redox Signaling, 12(10), 1191-1202. doi: 10.1089/ars.2009.2927

Hegde, A., Tamizhselvi, R., Manikandan, J., Melendez, A. J., Moochhala, S. M., & Bhatia, M. (2010). Substance P in polymicrobial sepsis: Molecular fingerprint of lung injury in preprotachykinin-A-/- mice. Molecular Medicine, 16, 188-198. doi: 10.2119/molmed.2009.00166

Zhang, J., Sio, S. W. S., Moochhala, S., & Bhatia, M. (2010). Role of hydrogen sulfide in severe burn injury-induced inflammation in mice. Molecular Medicine, 16(9-10), 417-424. doi: 10.2119/molmed.2010.00027

Tamizhselvi, R., Koh, Y.-H., Sun, J., Zhang, H., & Bhatia, M. (2010). Hydrogen sulfide-induces ICAM-1 expression and neutrophil adhesion to caerulein-treated pancreatic acinar cells through NF-κB and Src-family kinases pathway. Experimental Cell Research, 316, 1625-1636. doi: 10.1016/j.yexcr.2010.02.044

Koh, Y.-H., Tamizhselvi, R., & Bhatia, M. (2010). Extracellular signal-regulated kinase 1/2 and c-Jun NH2-terminal kinase, through nuclear factor-κB and activator protein-1, contribute to caerulein-induced expression of substance P and neurokinin-1 receptors in pancreatic acinar cells. Journal of Pharmacology & Experimental Therapeutics, 332(3), 940-948. doi: 10.1124/jpet.109.160416

Sio, S. W. S., Ang, S. F., Lu, J., Moochhala, S., & Bhatia, M. (2010). Substance P upregulates cyclooxygenase-2 and prostaglandin E metabolite by activating ERK1/2 and NF-κB in a mouse model of burn-induced remote acute lung injury. Journal of Immunology, 185(10), 6265-6276. doi: 10.4049/jimmunol.1001739

Sun, J., Ramnath, R. D., Tamizhselvi, R., & Bhatia, M. (2009). Role of protein kinase C and phosphoinositide 3-kinase-Akt in substance P-induced proinflammatory pathways in mouse macrophages. FASEB Journal, 23, 997-1010. doi: 10.1096/fj.08-121756

Zhang, H., Moochhala, S. M., & Bhatia, M. (2008). Endogenous hydrogen sulfide regulates inflammatory response by activating the ERK pathway in polymicrobial sepsis. Journal of Immunology, 181, 4320-4331.

Zhang, H., Hegde, A., Ng, S. W., Adhikari, S., Moochhala, S. M., & Bhatia, M. (2007). Hydrogen sulfide up-regulates substance P in polymicrobial sepsis-associated lung injury. Journal of Immunology, 179, 4153-4160.

Puneet, P., Hegde, A., Ng, S. W., Lau, H. Y., Lu, J., Moochhala, S. M., & Bhatia, M. (2006). Preprotachykinin-A gene products are key mediators of lung injury in polymicrobial sepsis. Journal of Immunology, 176, 3813-3820.

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