Go back to Faculty Members

RESEARCH | CURRICULUM VITAE | PUBLICATIONS      

bp1

 Name: BHASWATI PANDIT

 Email:   bp1

 Present Position:   Associate Professor

 Highest educational Qualification:  Ph.D.

 

Research:

 

Role of host genomics in determining susceptibility to tuberculosis

Traditionally, infectious diseases were textbook examples of “non-genetic diseases.”  But now beyond doubt it has been proven that genetic factors determine the susceptibility to various infectious diseases and their clinical courses upon infection.  About one third of world’s population is infected with M.Tb causing tuberculosis with India bout 1.8 million new cases annually. 5-10% of the infected individuals develop active disease at some point of his life, whereas 90% of infected individuals remain asymptomatic.  Individual with latent form of disease serves as a reservoir for the disease and is a major obstacle for controlling the disease. Studies with twins and genome wide analysis suggest that host genetics has strong role in determining susceptibility towards TB.

To address the issue of inter individual differences to disease susceptibility we are performing genomic studies to identify  host factors that independently or along with pathogen factors modulate course of  infection, disease progression and response to treatment. High throughput genotyping and sequencing platforms are used to identify variations in innate immune genes and other cytokines. We have identified that CXCL10 a chemokine is the most significantly altered cytokines in tuberculosis and correlates with severity of disease. Stimulation of CXCL10 expression by ESAT6 compared to Rv2031c reinforced the importance of CXCL10 in the active stage of infection. CXCL10 may, therefore, be considered as a potential biomarker of active phase of infection. In an exom-wide study we have identified a novel locus HLA-DRA associated with protection from tuberculosis.

We intend to understand the disease from different angles which includes genomics, transcriptomics studies and findings are functionally validated. We have recently expanded our study to other regions of India and developed strong collaboration with institutes pan India.

Molecular mechanisms underlying Congenital heart disease

Congenital Heart Disease (CHD) is a group of diseases with various anomalies in heart that occur during embryonic development. Molecular mechanisms of such defects include mutations in transcription factors regulating cardiac gene network, regulatory signaling proteins or sarcomeric proteins. MicroRNA dysfunction, epigenetics also contribute to CHD. The molecular etiology of congenital heart disease has been explored in great details, but lot more remains unanswered. We are interested in understanding the genetic alteration and its cellular effects that leads to different abnormal phenotypes of CHD like septal defect, valve stenosis, hypertrophic cardiomyopathy and many more. Our research focus is to investigate role of genetic variations, dysregulation of microRNA leading to altered gene expression in case of ASD. Different genomic tools are used for exploring such mechanisms.

Genetic and Epigenetic study of Systemic Lupus Erythematosus(SLE)

The major goal of this project is to understand the molecular basis of SLE among Indians. SLE is a heterogeneous autoimmune complex disease characterized by immune dysfunction. The hall mark of SLE is generation of auto antibodies. Till date no definite gene responsible for SLE has been identified, but several association studies and expression analysis in a genome wide manner have revealed role of interferon, cytokines triggering many signaling pathways in the immune system. I am interested in identification and mapping new genes for SLE.

 

Projects:

  • Genomics-driven Dissection of Susceptibility and Drug Resistance to Pulmonary Tuberculosis, with a Geographical Focus on NER (DBT funded)
  • Understanding the regulatory dynamics of tubercular granulomas through genomic and proteomic analyses: implications for latency and re-activation  (DBT funded, completed)
  • Exploring underlying Molecular mechanisms of defects in congenital heart disease
  • Understanding immunogenetics of Systemic Lupus Erythematosus  among Indians

Selected Publications:

  • Bhattacharyya C, Majumder PP, Pandit B, An exomwide association study of pulmonary tuberculosis patients and their asymptomatic household contacts, Infection Genetics & Evolution, (2019) 71:76-81.
  • Bishwal SC, Das MK, Badireddy VK, Dabral D, Das A et.al, Sputum Proteomics Reveals a Shift in Vitamin D-binding Protein and Antimicrobial Protein Axis in Tuberculosis Patients, Scientific Report, (2019) 31;9(1):1036. 
  • Bhattacharyya C, Majumder PP, Pandit B, CXCL10 is overexpressed in active Tuberculosis patients compared to M. tuberculosis-exposed household contacts, Tuberculosis (2018) 109:8-16.
  • Agrawal N, Bhattacharyya C, Mukherjee A, Ullah U, Pandit B, Rao  KVS,  Majumder PP, Dissecting host factors that regulate the early stages of tuberculosis infection, Tuberculosis, (2016)100:102-113.
  • Das MK, Bishwal SC, Das A, Dabral D, Badireddy VK, Pandit B, Varghese GM, Nanda RK, Deregulated tyrosine-phenylalanine metabolism in pulmonary tuberculosis patients, J Proteome Research (2015) 14(4): 1947-56.
  • Pandit B, Sarkozy A, Pennacchio LA et.al.Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy- Nature Genetics (2007) 39(8):1007-1012.
  • Tartaglia M, Pennacchio LA, Zhao C, Yadav KK., Fodale V, Sarkozy A, Pandit B, Oishi K, Martinelli S et. al. Gain-of-function SOS1 mutations cause a distinctive form of Noonan syndrome, Nature Genetics (2007) 39(1):75-79.
  • Pandit B, Ahn GS , Hazard SE, Gordon D, Patel SB, A detailed Hapmap of the STSL locus spanning 69kb; Differences between Caucasians and African-Americans, BMC Medical Genetics (2006) 7(1): 13.