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Dr. Prasenjit Guchhait

Professor
E-mail: prasenjit at rcb dot res dot in

  • PhD 1998, Banaras Hindu University
  • Postdoc at Baylor College of Medicine, USA
  • Instructor at Baylor College of Medicine, USA
  • Assistant Professor at Baylor College of Medicine, USA
  • Associate Professor at Regional Centre for Biotechnology, India

Our Disease Biology laboratory is focused on elucidating:

1) (A)Mechanism of systemic inflammation in hemolytic diseases including paroxysmal nocturnal hemoglobinuria (PNH), hemolytic uremic syndrome (HUS), thalassemia and sickle cell disease (SCD), with a focus on activation of immune cells (mainly innate cells) by platelet and its molecules. Also we study the association of other clinical events such as hyper-coagulation, thrombosis and complement activation in the pathogenesis of systemic inflammations, our pubs, Thrombosis Haemostasis 2009, 2010, 2011; Haematologica 2015; Blood 2015; PLoS One 2016, 2017; Clinical Immunology 2017; European J Immunology 2018; J Immunology Research 2019; Clinical Experimental Immunology 2019. Using mice models and patients’ samples, we are currently studying the interplay between leukocytes and platelets to understand more insights into the prevalence and severity of systemic inflammation and also investigating the altered immune responses (innate and adaptive) in these hemolytic disorders. (B) Mechanism of systemic inflammation in patients with autoimmune disorders such as atypical hemolytic uremic syndrome (aHUS) and systemic lupus erythematosus (SLE): with a focus on the role of complement factors such as factor H (FH) and FHR in the activation of C3b and development of systemic inflammation, our pubs, Immunology 2017, J Clinical Immunology 2019, Blood Cells Molecules and Diseases 2019. (C) Mechanism of systemic as well as lung inflammation, and lung fibrosis In type-2 diabetes (T2D): with a focus on the interplay between platelet and leukocytes in the pathogenesis of inflammations, using transgenic mice model of T2D as well as patients’ samples. (D) Mechanism of systemic inflammation in accidental trauma patients: we are studying the role of necrotic/apoptotic tissues at the site of injury in the development of systemic inflammations. We are investigating why only 17-20% patients develop systemic inflammations.

2) (A) Mechanism of pulmonary edema (inflammation) and intravascular thrombosis (clot formation) in patients (mainly travellers to high-altitudes) with high altitude pulmonary edema (HAPE) and acute mountain sickness (AMS). Unlike the travellers, the native highlanders including Tibetans are living normally at higher altitudes under extreme conditions (where partial pO2 pressure less than 40% compared to sea-level). Recently we have described that the novel mutations (C12G and G380C) in EGLN1 gene (which encodes Prolyl Hydroxylase-2 (PHD2), the negative regulator of hypoxia inducible factor (HIF)-1α (master oxygen sensor in our body), supports the adaptation of the native Tibetans at high-altitudes. Basically, these gain-in-function mutations help in maintenance of normal erythropoiesis in these highlanders, our pubs, Nature Genetics 2014; J Molecular Medicine 2017. Further, we are investigating how Tibetans highlanders are protected from edema and thrombosis: with a focus on platelet-immune cells interactions that trigger edema and thrombosis among travellers but not in native Tibetan highlanders, our pub, World Cong on Mountain Medicine 2018. Further we are investigating new insights into it and also developing new therapeutic strategy to inhibit aggravated immune response in patients with HAPE and AMS. (B) Mechanism for high prevalence and severity of T2D among highlanders, migrate from high to lower altitudes or sea levels. We are investigating the new insights into the crosstalk between hypoxia-responsive factors and metabolites (mainly glucose/fat oxidation pathways) and association with the pathogenesis of T2D among migrants from high to low altitudes.

3) (A) Mechanism of thrombocytopenia in Dengue virus (DV) infection: we have shown that the frequency/degree of platelet activation by DV is the crucial determinant of thrombocytopenia in Dengue patients, our pub, Scientific Report 2017. Further we are investigating the new insights into mechanism of thrombocytopenia with a focus on the interaction between platelet and leukocytes. (B) Molecular mechanism of rapid replication and propagation of Dengue and Japanese Encephalitis virus (JEV) in host: with a focus on the role of activated-platelet and its cytokine, called platelet factor 4 (PF4). PF4 inhibits interferon (IFN) -signaling pathway and helps in viral propagation, our pub, EBioMedicine 2019. Further, we are investigating new insights into above mechanism with a focus on host immune responses against viral infections using mice models of DV and JEV, and patients’ samples. Also we are developing small molecules inhibitors against PF4 and its receptor CXCR3 for the treatment of these viruses using above mice models.

We use high-end molecular and cell biology tools including flowcytometry, microscopy, genomics and proteomic approaches, and transgenic animal models and patients’ samples of related diseases for addressing the above research problems.

We search for biomarkers as well as potential molecular targets to develop therapeutics.

  • Amrita Ojha
    Senior Research Fellow
    amrita.ojha@rcb.res.in
  • Angika Bhasym
    Senior Research Fellow
    angika.bhasym@rcb.res.in
  • Sulagna Bhattacharya
    Senior Research Fellow
    sulagna.sb@rcb.res.in
  • Srimali Nishith Maheshbhai
    Senior Research Fellow
    nishith@rcb.res.in
  • Saibal Saha
    Junior Research Fellow
    saibal@rcb.res.in
  • Sakshi Agarwal
    Junior Research Fellow
    sakshi.agarwal@rcb.res.in
  • Anamika Singh
    Junior Research Fellow
    sakshi.agarwal@rcb.res.in
  1. Bhasym A, Bhakuni T and Guchhait P. (2019) Elevated surface-bound complement factor-H alters the function of platelets and monocytes in FHR1/3-null healthy individuals. Blood Cells Molecules Diseases | Doi.org/10.1016/j.bcmd.2019.102349
  2. Bhasym A, Annarapu GK, Saha S, Shrimali N, Gupta S, Seth T, Guchhait P. (2019) Neutrophils develop rapid proinflammatory response after engulfing Hb-activated platelets under intravascular hemolysis. Clin Exp Immunol | Doi: 10.1111/cei.13310
  3. Bhakuni T, Singhal R, Aannarapu GK, Sharma A, Mahapatra M, Saxena R, Guchhait P (2019) Unique case of autoantibody mediated inactivation of ADAMTS13 in an Indian TTP patient. Blood Cells Molecules Diseases | 77:29-33
  4. Bhasym A, Gurjar BS, Sriharsha TM, Bhasym A, Prabhu S, Puraswani M, Khandelwal P, Saini H, Saini S, Verma AK, Chatterjee P, Bal V, George A, Sharma A, Hari P, Sinha A, Bagga A, Rath S, Guchhait P (2019) Altered Peripheral Blood Leucocyte Phenotype and Responses in Healthy Individuals with Homozygous Deletion of FHR1 and FHR3 Gene. J Clinical Immunology | Doi.org/10.1007/s10875-019-00619-2
  5. R Singhal, DK Rathore, T Bhakuni, T Seth, P Guchhait (2019) Absence of Nonclassical Monocytes in Hemolytic Patients : Free Hb and NO-Mediated Mechanism Journal of Immunology Research | doi.org/10.1155/2019/1409383
  6. Ojha A, Bhasym A, Mukherjee S, Annarapu GK, Bhakuni T, Akbar I, Seth T, Vikram NK, Vrati S, Basu A, Bhattacharyya S, Guchhait P. Platelet factor 4 promotes rapid replication and propagation of Dengue and Japanese encephalitis viruses. EBioMedicine 2018 | 39:332-347
  7. Singhal R, Chawla S, Batra H, Gupta S, Ojha A, Rathore DK, Seth T, Guchhait P (2018) Engulfment of Hb-activated platelets differentiates monocytes into pro-inflammatory macrophages in PNH patients. Eur J Immunol. [Epub ahead of print]
  8. Gurjar BS, Sriharsha TM, Bhasym A, Prabhu S, Puraswani M, Khandelwal P, Saini H, Saini S, Verma AK, Chatterjee P, Gucchait P, Bal V, George A, Rath S, Sahu A, Sharma A, Hari P, Sinha A, Bagga A. (2018) Characterization of genetic predisposition and autoantibody profile in atypical hemolytic uremic syndrome. Immunology
  9. Tashi T, Reading N S, Wuren T, Zhang X, Moore L G, Hu H, Tang F, Shestakova A, Lorenzo F, Burjanivova T, Koul P, Guchhait P, Wittwer C T, Julian C G, Shah B, Huff C D, Gordeuk V R, Prchal J T, Ge R (2017) Gain-of-function EGLN1 prolyl hydroxylase (PHD2 D4E:C127S)in combination with EPAS1 (HIF-2α) polymorphism lowershemoglobin concentration in Tibetan highlanders J Mol Med 95-665
  10. Ojha A , Nandi D, Batra H, Singhal R, Annarapu G. K., Bhattacharyya. S, Seth T, Dar L, Medigeshi G. R., Vrati S, Vikram N. K & Guchhait P (2017) Platelet activation determines the severity of thrombocytopenia in dengue infection Sci Rep 7: 41697
  11. Singhal R, Chawla S, Rathore D K, Bhasym A, Annarapu G K, Sharma V, Seth T, Guchhait P (2016)Development of pro-inflammatory phenotype in monocytes after engulfing Hb-activated platelets in hemolytic disorders.. Clinical Immunology 12: 007
  12. Annarapu GK, Singhal R, Gupta A, Chawla S, Batra H, Seth T, Guchhait P (2016) HbS Binding to GP1ba Activates Platelets in Sickle Cell Disease.. PLoS One 11:e0167899
  13. Annarapu GK, Singhal R, Peng Y, Guchhait P. (2016) Inhibition of Hb binding to GP1bα abrogates Hb-mediated thrombus formation on immobilized VWF and collagen under physiological shear stress. PLoS One. 11:e0154276
  14. Singhal R, Annarapu GK, Pandey A, Chawla S, Ojha A, Gupta A, Cruz MA, Seth T, Guchhait P. (2015)  Hemoglobin interaction with GP1ba induces platelet activation and apoptosis: a novel mechanism associated with intravascular hemolysis. Haematologica. pii: haematol.132183. [Epub ahead of print]
  15. Da Q, Teruya M, Guchhait P, Teruya J, Olson JS, Cruz MA (2015)  Free hemoglobin increases von Willebrand factor-mediated platelet adhesion in vitro: implications on circulatory devices. Blood. pii: blood-2015-05-648030. [Epub ahead of print]
  16. Pandey A, Chawla S, Guchhait P (2015)  Type-2 diabetes: Current understanding and future perspectives. IUBMB Life 67:506
  17. Lorenzo FR, Huff C, Myllymäki M, Olenchock B, Swierczek S, Tashi T, Gordeuk V, Wuran T, Li GR, McClain DL, Khan TM, Koul PA, Guchhait P, Salama ME, Xing J, Semenz GL, Liberzon E, Wilson A, Simonson TS, Jorde LB, KaelinJr WG, Koivunen P, Prchal JT. (2014) A genetic mechanism for Tibetan high-altitude adaptation. Nature Genetics 46:951.
  18. Zhou Z, Thiagarajan P, Udden MA, Lopez JA, Guchhait P. (2011) Membrane sulfatide plays a crucial role in the sickle erythrocytes adhesion to matrix and endothelial ligands. Thrombosis Haemostasis105:1046.
  19. Zhou Z, Han H, Cruz MA, Jose JA, Dong JF, Guchhait P. (2009) Hemoglobin blocks von Willebrand factor proteolysis by ADAMTS-13: a mechanism associated with sickle cell disease. Thrombosis Haemostasis 101 (6):1070.
  20. Guchhait P, Shrimpton C, Honke K, Rumbaut R, Lopez JA, Thiagarajan P. (2008) Effects of an anti-sulfatide single-chain antibody probe on platelet function. Thrombosis Haemostasis 99(3):552.

Dr. Prasenjit Guchhait
Professor
Regional Centre for Biotechnology
NCR Biotech Science Cluster
3rd Milestone, Faridabad-Gurgaon Expressway
P.O. Box No. 3, Faridabad - 121 001
Haryana (NCR Delhi), India
E-mail: prasenjit at rcb dot res dot in
Phone: 91 129-2848821

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