- Postdoctoral training- Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, 2013
- Ph.D.- University of Wisconsin-Madison, WI, USA, 2010
- M.S.- Wichita State University, KS, USA, 2006
- B.V.Sc & A.H- West Bengal University of Animal and Fishery Sciences, India, 2003
Education & Training
Vasamsetti SB, Florentin J, Coppin E, Stiekema L, Zheng KH, Nisar MU, Levinthal D, Rojas M, Stroes ES, Kim K, Dutta P. Sympathetic neuronal activation triggers myeloid progenitor proliferation and differentiation. Immunity. 2018. pii: S1074-7613(18)30240-1. doi: 10.1016/j.immuni.2018.05.004. PMID: 29958804.
Florentin J, Coppin E, Vasamsetti SB, Zhao J, Tai YY, Tang Y, Zhang Y, Watson A, Sembrat J, Rojas M, Vargas SO, Chan SY*, Dutta P*. Inflammatory macrophage expansion in pulmonary hypertension depends upon mobilization of blood-borne monocytes. J of Immunol. 2018. (Epub ahead of print). PMID: 29632145. *Co-senior authors.
Coppin E, Florentin J, Vasamsetti SB, Arunkumar A, Sembrat J, Rojas M, Dutta P. Splenic hematopoietic stem cells display a pre-activated phenotype. Immunol Cell Biol. 2018 (Epub ahead of print). IMID: 29526053
Dutta P, Hoyer FF, Sun Y, Iwamoto Y, Tricot B, Weissleder R, Magnani JL, Swirski FK, Nahrendorf M. E-selectin inhibition mitigates splenic HSC activation and myelopoiesis in hypercholesterolemic mice with myocardial infarction. Atheroscler Thromb Vasc Biol 2016 Sep;36(9):1802-8. PMCID: PMC5001901
Bracamonte-Baran W, Florentin J, Zhou Y, Jankowska-Gan E, Haynes WJ, Zhong W, Brennan TV, Dutta P, Class FH, va Rood JJ, Burlingham WJ. Modification of host dendritic cells by microchimerism-derived extracellular vesicles generates split tolerance. Proc Natl Acad Sci Jan 31;114(5):1099-1104. PMCID: PMC5293109
Sager HB*, Dutta P*, Dahlman JE, Borodovsky A, Fitzgerald K, Heidt T, Courties G, Wojtkiewicz GR, Iwamoto Y, Sebas M, Khan OF, Xing Y, Shaw TE, Libby P, Swirski FK, Langer R, Weissleder R, Anderson DG, Nahrendorf RNAi targeting multiple cell adhesion molecules reduces immune cell recruitment and vascular inflammation after myocardial infarction. Sci Transl Med. 2016 Jun 8;8(342):342ra80 PMID: 27280687. *Equal contribution
Dutta P, Sager H, Stengel K, Naxerova K,……Libby P, Hiebert S, Scadden D, Swirski FK, Weissleder R, Nahrendorf M. 2015. Myocardial infarction activates CCR2+ hematopoietic stem cells. Cell Stem Cell 16: 477-87.
Correspondence: Partha Dutta (dutta.partha@mgh.harvard.edu) and Matthias Nahrendorf (mnahrendorf@mgh.harvard.edu)
Dutta, P., F. F. Hoyer, L. S. Grigoryeva, H. B. Sager, F. Leuschner, G. Courties, A. Borodovsky, T. Novobrantseva, V. M. Ruda, K. Fitzgerald, Y. Iwamoto, G. Wojtkiewicz, Y. Sun, N. Da Silva, P. Libby, D. G. Anderson, F. K. Swirski, R. Weissleder, and M. Nahrendorf. 2015. Macrophages retain hematopoietic stem cells in the spleen via VCAM-1 in atherosclerosis. Journal of Experimental Medicine 212: 497-512.
Correspondence: Partha Dutta (dutta.partha@mgh.harvard.edu) and Matthias Nahrendorf (mnahrendorf@mgh.harvard.edu)
Sager HB, T. Heidt, M. Hulsmans, Dutta, G. Courties, M. Sebas, G. R. Wojtkiesicz, B. Tricot, Y. Iwamoto, Y. Sun, R. Weissleder, P. Libby, F.K. Swirski, M. Nahrendorf. 2015. Targeting interleukin-1beta reduces leukocyte production after acute myocardial infarction. Circulation.
Dutta, P., G. Courties, Y. Wei, F. Leuschner, R. Gorbatov, C. S. Robbins, Y. Iwamoto, B. Thompson, A. L. Carlson, T. Heidt, M. D. Majmudar, F. Lasitschka, M. Etzrodt, P. Waterman, M. T. Waring, A. T. Chicoine, A. M. van der Laan, H. W. Niessen, J. J. Piek, B. B. Rubin, J. Butany, J. R. Stone, H. A. Katus, S. A. Murphy, D. A. Morrow, M. S. Sabatine, C. Vinegoni, M. A. Moskowitz, M. J. Pittet, P. Libby, C. P. Lin, F. K. Swirski, R. Weissleder, and M. Nahrendorf. 2012. Myocardial infarction accelerates atherosclerosis. Nature 487: 325-329.
Heidt, T., H. B. Sager, G. Courties, Dutta, Y. Iwamoto, A. Zaltsman, C. von Zur Muhlen, C. Bode, G. L. Fricchione, J. Denninger, C. P. Lin, C. Vinegoni, P. Libby, F. K. Swirski, R. Weissleder, and M. Nahrendorf. 2014. Chronic variable stress activates hematopoietic stem cells. Nature Medicine 20: 754-758.
Leuschner, F*., Dutta*, R. Gorbatov, T. I. Novobrantseva, J. S. Donahoe, G. Courties, K. M. Lee, J. I. Kim, J. F. Markmann, B. Marinelli, P. Panizzi, W. W. Lee, Y. Iwamoto, S. Milstein, H. Epstein-Barash, W. Cantley, J. Wong, V. Cortez-Retamozo, A. Newton, K. Love, P. Libby, M. J. Pittet, F. K. Swirski, V. Koteliansky, R. Langer, R. Weissleder, D. G. Anderson, and M. Nahrendorf. 2011. Therapeutic siRNA silencing in inflammatory monocytes in mice. Nature Biotechnology 29: 1005-1010. * Equal contribution authors
Dutta, P., M. Dart, D. A. Roenneburg, J. R. Torrealba, and W. J. Burlingham. 2011. Pretransplant immune-regulation predicts allograft tolerance. Am J Transplant 11: 1296-1301.
Dutta, P., M. Molitor-Dart, J. L. Bobadilla, D. A. Roenneburg, Z. Yan, J. R. Torrealba, and W. J. Burlingham. 2009. Microchimerism is strongly correlated with tolerance to noninherited maternal antigens in mice. Blood 114: 3578-3587.
Cardiovascular disease is the leading cause of death in developed countries. Inflammation aggravates outcome of cardiovascular disease including atherosclerosis and infarct healing after myocardial infarction (MI) (Leuschner* and Dutta* et al., Nature Biotechnology, 2011). During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaques in the arterial wall and cause their rupture, thus triggering myocardial infarction and stroke. Survivors of acute coronary syndromes have a high risk of recurrent events for unknown reasons. We showed that the systemic response to ischemic injury aggravates chronic atherosclerosis (Dutta et al., Nature, 2012). After myocardial infarction or stroke, ApoE-/- mice developed larger atherosclerotic lesions with a more advanced morphology and inflammation. This disease acceleration persisted over many weeks and was associated with markedly increased monocyte recruitment.
One of our current research interests focuses on immunology of cardiovascular disease. We are investigating how myeloid cells, such as monocytes and macrophages, induce inflammation in metabolic disease such as type II diabetes and cardiovascular disease such as myocardial infarction. The ultimate goal of the lab is to develop potential therapeutic avenues to check generation of myeloid cells in the bone marrow and spleen, and recruitment of myeloid cells to sites of inflammation such as adipose tissue and the myocardium. We are also keenly interested to investigate differential functions of tissue resident and monocyte-derived macrophages in steady state and disease.