ICMR-National Institute of Cholera and Enteric Diseases

आई सी एम आर - राष्ट्रीय कॉलरा और आंत्र रोग संस्थान

Department of Health Research, Ministry of Health and Family Welfare, Government of India
स्वास्थ्य अनुसंधान विभाग, स्वास्थ्य और परिवार कल्याण मंत्रालय, भारत सरकार
WHO Collaborating Centre For Research and Training On Diarrhoeal Diseases

NICED : Scientists

Dr. Moumita Bhaumik Ghosh

Dr. Moumita Bhaumik (Ghosh)


General Information
Name Dr. Moumita Bhaumik (Ghosh)
Designation Scientist C
Date of joining ICMR 06 November 2017
Date of joining present post 06 November 2017
Discipline Immunology
Email : drmoumitabhaumik@gmail.com
Academic Qualification  
Graduation Zoology, University of Calcutta
Post Graduation Biophysics and Molecular biology. University of Calcutta
Doctoral Biophysics and Molecular biology, CSIR-IICB, Kolkata


Research Experience

My doctoral research experience revolved around the pathogenesis of the Leishmania infection. Leishmania, a protozoan parasite causing the disease Kala-azar exhibit a pronounced tropism for macrophages. Once, the parasite is well established, it causes aberrant changes in macrophage property and function. My study was designed to understand the 'complex rules' by which Leishmania parasites modulate the biological functions of the macrophage affecting the antileishmanial immune repertoire. All the studies were restricted on three aspects of cell biology of Leishmania infected macrophage - the macrophage membrane function, effective immune stimulation by antileishmanial drugs and antigen processing and presentation of exogenous antigen. Thus, it was shown how Leishmania parasites modulate the macrophage function which may have significant impact on the immunopathology of Leishmaniasis.

Research Interest

I thrust my interest on commensal bacteria which constitutes an ecosystem inside our gut, known as "microbiome". It has a protective, metabolic and trophic functions thus regulating various physiological system of our body. For which, the body requires keyinduction and maintenance signals from microbiome, many of them are yet to be discovered. I would pursue my studies on the following aspects of gut microbiotaand host interactionto find out the key factor. First, the impact of microbiome on immune system of the host. Second, the mechanism by which it orchestrates the physiology of the host. Third, the environmental factorsand antibiotics on perturbing gut microbiome, affecting host physiology.


  1. A. K. Memorial medal for first class first in B.Sc(Zoology) from University of Calcutta (2004)



  1. Ghosh M, Roy K, Das Mukherjee D, Chakrabarti G, Roy Choudhury K, Roy S. Leishmania donovani infection enhances lateral mobility of macrophage membrane protein which is reversed by liposomal cholesterol. PLoS Negl Trop Dis. 2014 Dec 4;8(12):e3367. .  Pubmed
  2. Roy K, Naskar K, Ghosh M, Roy S. Class II MHC/peptide interaction in Leishmania donovani infection: implications in vaccine design. J Immunol. 2014 Jun 15;192(12):5873-80 Pubmed


  1. Ghosh M, Roy K, Roy S. Immunomodulatory effects of antileishmanial drugs. J Antimicrob Chemother. 2013 Dec;68(12):2834-8  Pubmed
  2. Roy K, Ghosh M, Pal TK, Chakrabarti S, Roy S. Cholesterol lowering drug may influence cellular immune response by altering MHC II function. J Lipid Res. 2013 Nov;54(11):3106-15.   Pubmed
  3. Ghosh M, Solanki AK, Roy K, Dhoke RR, Ashish, Roy S. Carrier protein influences immunodominance of a known epitope: implication in peptide vaccine design. Vaccine. 2013 Sep 23;31(41):4682-8.   Pubmed


  1. Datta S, Manna M, Khanra S, Ghosh M, Bhar R, Chakraborty A, Roy S. Therapeutic immunization with radio-attenuated Leishmania parasites through i.m. route revealed protection against the experimental murine visceral leishmaniasis. Parasitol Res. 2012 Jul;111(1):361-9.  Pubmed


  1. Bhattacharya P, Gupta G, Majumder S, Adhikari A, Banerjee S, Halder K, Majumdar SB, Ghosh M, Chaudhuri S, Roy S, Majumdar S. Arabinosylated lipoarabinomannan skews Th2 phenotype towards Th1 during Leishmania infection by chromatin modification: involvement of MAPK signaling. PLoS One. 2011;6(9):e24141. Pubmed


  1. 8. Banerjee S, Ghosh J, Sen S, Guha R, Dhar R, Ghosh M, Datta S, Raychaudhury B, Naskar K, Haldar AK, Lal CS, Pandey K, Das VN, Das P, Roy S. Designing therapies against experimental visceral leishmaniasis by modulating the membrane fluidity of antigen-presenting cells. Infect Immun. 2009 Jun;77(6):2330-42. Pubmed