People : Scientific : Faculty & Scientists

DR. AMIT KUMAR PANDEY, Ph.D. 

Assistant Professor
+91-129-3087322  (911292876357)
amitpandey [at] thsti [dot] res [dot] in
Posdoctoral Fellow from University of Nebraska-Lincoln, Nebraska, USA
Posdoctoral Fellow from University of Massachusetts Medical School, Worcester, Massachusetts, USA
Ph.D. Indian Veterinary Research Institute, Izatnagar, U.P., India
M.Sc. (Animal Biotechnology), National Dairy Research Institute, Karnal, India
B.V.Sc and A.H, Orissa University of Agriculture and Technology, Bhubaneswar, India

Present Research Interest

Mycobacterium tuberculosis (Mtb) the causative agent of tuberculosis (TB) is responsible for 2 million deaths every year worldwide. The pathogen’s ability to replicate and survive inside the macrophage, in the very vacuole that has been designed by the host to kill pathogens, has been a great challenge in designing efficient therapeutic or prophylaxis strategies. The environment inside the Mtbintracellular niche is broadly defined by the nature and availability of the various nutrients and the redox state inside it. The successful adaptation of Mtb to the nutritional deprivation and immune insults found in the host niche makes this organisms one of the most successful parasite in the history of mankind. A long history of co-evolution and the chronic nature of the disease has led to a very complicated host pathogen relationship. This relationship, at best can be defined as a “truce” in the war going on between the host and the pathogen. The above facts have led to the hypothesis that Mtb could be heavily dependent on the host for its survival inside a very hostile intracellular niche. A better understanding of this complex relationship would provide us with information that could lead to an elaborate repertoire of potential gene that can be targeted for a better therapeutics against tuberculosis. Studies in our lab primarily focusses on understanding the biology of Mtb pathogenesis with specific focus on host pathogen interaction.
My work at Dr Sassetti’s lab lead to the finding that Mtb could metabolize cholesterol and preferentially use different parts of the molecule for energy and biosynthetic purposes. The finding that cholesterol utilization is essential for the maintenance of the persistent state of Mtb infection is very intriguing. Studying regulation of cholesterol metabolism in Mtb and its implications on mycobactrial pathogenesis would be the immediate focus of the lab. It would be interesting to see if there are other host derived macro-molecules that are critical for Mtb infection. Understanding those pathways might help us identify new target for a better therapeutics.

Regulation of cholesterol metabolism in Mycobacterium tuberculosis

Genetic requirement of Mycobacterium tuberculosis growth in cholesterol under hypoxia

Identifying genes specific for cholesterol toxicity independent of propionate toxicity

 

Honour & Awards

  • Ramalingaswami Fellowship, 2010-11

  • Transcriptional induction of methylcitrate cycle enzymes is necessary for M. tuberculosis to metabolize cholesterol during intracellular growth. Jennifer E.Griffin*, Amit K. Pandey*,Valerie Mizrahi, John D. McKinney, and Christopher M. Sassetti. 2010. Manuscript under preparation.
  • NOD2, RIP2 and IRF5 Play a Critical Role in the Type I Interferon Response to Mycobacterium tuberculosis. Amit K. Pandey, Yibin Yang, Zhaozhao Jiang, Sarah M. Fortune, Francois Coulombe, Marcel A. Behr, Katherine A. Fitzgerald, Christopher M. Sassetti and Michelle A. Kelliher. 2009. PLoS Pathogen. PLoS Pathog. 2009 Jul;5(7):e1000500. Epub 2009 July3. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2698121&blobtype=pdf
  • Increase NOD2-mediated recognition of N-glycolylated muramyl dipeptide. Francois Coulombe, Maziar Divangahi, Frederic Veyrier, James Gleason, Yibin Yang, Michelle A. Kelliher, Amit K. Pandey, Christopher M. Sassetti, Michael B. Reed and Marcel A. Behr. Journal of Expt. Med. (2009). Aug 3;206(8):1709-16. Epub 2009 Jul 6.http://jem.rupress.org/cgi/reprint/jem.20081779v1
  • Phthiocerol dimycocerosate transport is required for resisting IFN-γ-independent immunity. Jeffrey P. Murry, Amit K. Pandey, Christopher M. Sassetti, and Eric J. Rubin. 2009. Journal of Infectious Diseases. (2009). Sep 1;200(5):774-82.
  • Role of Cholesterol in Mycobacterium tuberculosis infection. Maurine D Miner, Jennifer C Chang, Amit K Pandey, Christopher M Sassetti and David R Sherman. Indian Journal of Exp. Biol. (2009). June; 47: 407-11.
  • Nitrile-inducible gene expression in mycobacteria. Amit K. Pandey, Sahadevan Raman, Rose Proff, Swati Josh, C.M. Kang, Eric J. Rubin, Robert N. Husson and Christopher M. Sassetti. Tuberculosis (Edinb) (2009).Jan;89(1):12-16
  • Mycobacterial persistence requires the utilization of host cholesterol. Amit K. Pandey and Christopher M Sassetti. Proc Natl Acad Sci. U S A (2008). March 18; 105(11):4376-80. http://www.pnas.org/content/105/11/4376.full.pdf+html
  • NOD2 pathway activation by MDP or Mycobacterium tuberculosis infection involves the stable polyubiquitination of Rip2. Yibin Yang, Catherine Yin, Amit Pandey, Derek Abbott, Christopher Sassetti and Michelle A. Kelliher. J. Biol. Chem.(2007) Dec 14; 282(50):36223-9. http://www.jbc.org/cgi/reprint/282/50/36223
  • Characterization of mycobacterial virulence genes through genetic interaction mapping. Swati Joshi, Amit K. Pandey, Nicole Capite, Sarah M. Fortune, Eric J. Rubin, and Christopher M. Sassetti. Proc Natl Acad Sci. U S A.(2006). Aug 1; 103(31):11760-5. http://www.pnas.org/content/103/31/11760.full.pdf+html
  • Identification of Mycobacterium marinum macrophage infection mutants. Parmod K. Mehta*, Amit K. Pandey*, Selvakumar Subbian, Mustapha M. Samarkandi, Suat L.G. Cirillo and Jeffery D. Cirillo. Microb Pathog.(2006). Apr;40(4):139-51.

*contributed equally to this work.