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Mentor Bio
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Vishwa Dixit, DVM, Ph.D.
Head, Laboratory of Neuroendocrine-Immunology, PBRC.
Adjunct Assistant Professor, Department of Microbiology, Immunology and Parasitology, LSU-Health Science Center, New Orleans
Assistant Professor
Department/Laboratory:
Neuroendocrine Immunology
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Phone:
(225) 763-2719
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Fax:
(225) 763-0261 |
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E-mail
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Education:
1994- Doctor of Veterinary Medicine, CCS Haryana Agricultural University- Hisar, India
1996 - Masters of Veterinary Science, Animal Physiology, CCS Haryana Agricultural University- Hisar, India.
2000 - Ph.D, Physiology. University of Hannover, Institut Fuer Tierzucht, Mariensee, Germany and HAU-India.
2001 to 2005 - Post Doc Fellow - NIH.
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Research
Interests:
Focus: Cellular and molecular mechanisms of aging and obesity-related decline in immunity and aberrant inflammatory response
A major research emphasis of this laboratory is to study the dialogue between adipose and immune cells in relation to aging and obesity. We call this emerging area as Adipoimmunology. We define Adipoimmunology as area of research devoted to studying the interactions between adipocytes and immune cell subsets via their secreted products and cell-cell interactions within adipose and lymphoid tissue microenvironment and consequences of these interactions during disease states of obesity (insulin resistance, infection and cancer) and/or aging (immune deficiency and autoimmunity).
As we grow older, thymus, an immune-organ that produces infection and cancer fighting T cells is converted into adipose-tissue and cannot effectively generate T cells. Dogma dictates that adipocytes or fat cells “infiltrate/invade” the thymus to “fill space” in absence of T cells. However, Laboratory of Neuroendocrine-Immunology at PBRC has challenged this belief. The latest research work from Dixit Lab, employed genetic fate-mapping and discovered that a subset of specialized thymic epithelial cells, that are vital for T cell development, trans-differentiate, loose their function and become fat cells. Considering that hematopoietic stem cells in bone marrow develop into T cells only in thymus, loss of thymic epithelial cells and emergence of adipocyte leads to age-related decline in immune function and increased risk of influenza, shingles, infections, cancer and vaccination failures. The ongoing research in this laboratory is focused on understanding the basic mechanisms of abnormal-adipocyte formation in immune-organs in an effort to develop future therapeutic strategies to strengthen immune system. Dixit Lab is also translating these basic research findings to the clinic by investigating if pro-longevity experimental intervention called caloric restriction can enhance immune function in humans. This study called “CALERIE” is expected to be complete in year 2013 and would be the first controlled randomized clinical trial to investigate the impact of caloric restriction on reversing or retarding the aging of thymus in humans.
As the continued deposition of adipocytes in the immune microenvironment is detrimental, similarly, the increase in immune cells in adipose tissue depots during obesity leads to type-2 diabetes. Working on the interface of Immunobiology, aging and obesity the Laboratory of Neuroendocrine-Immunology, has found that aberrant expansion of immune cells can alter adipocyte biology and may play an important role in various diseases. It is currently believed that the presence of immune cells called macrophages in the adipose tissue is responsible for production of pro-inflammatory cytokines that cause insulin resistance. This laboratory at PBRC has discovered that in addition to macrophages, the adipose tissue in obese animals and humans harbors various activated immune cell subsets, including effector-T cells that produce excessive amount of cytokines. These findings have direct implications for understanding the origin of the pro-inflammatory state of obesity, hence providing vital insights into the mechanism of type-2 diabetes and immunodeficiency.
Research in this laboratory is supported by the National Institutes of Health (R01AG031797), Pilot Awards from NIDDK funded CNRU grant (1P20 RR02/1945) and Coypu Foundation.
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Selected
Publications:
(from 35)
Yang H, Youm YH, Vandanmagsar B, Rood J, Kumar KG, Butler AA and Dixit VD. (2009). Obesity accelerates thymic aging. Blood, Aug 31. [Epub ahead of print]
Yang H, Youm YH and Dixit VD. (2009). Inhibition of Thymic Adipogenesis by Caloric Restriction is coupled with Reduction in Age-related Thymic Involution. J. Immunol. Sep 1;183(5):3040-52.
Yang H, Youm YH, Sun Y, Rim JS, Galban C, Vandanmagsar B, Dixit VD. (2009) Axin expression in thymic stromal cells contributes to age-related increase in thymic adiposity and associated with reduced thymopoiesis independently of ghrelin signaling. J. Leukoc Biol. 85: 928-938.
Youm YH, Yang H, Sun Y, Smith RG, Manley NR, Vandanmagsar B and Dixit VD. (2009) Deficient ghrelin receptor mediated signaling compromises thymic stromal cell microenvironment by accelerating thymic adiposity. J. Biol. Chem. 284: 7068-7077.
Kumar KG, Sutton GM, Dong JZ, Roubert P, Plas P, Halem HA, Culler MD, Yang H, Dixit VD, Butler AA. (2009) Analysis of the therapeutic functions of novel melanocortin receptor agonists in MC3R- and MC4R-deficient C57BL/6J mice. Peptides. 2009 Oct;30(10):1892-900.
Dixit VD, Yang H, Cooper-Jenkins A, Giri BB, Patel K, Taub D. (2009) Reduction of T cell-Derived Ghrelin Enhances Proinflammatory Cytokine Expression: Implications for Age-Associated Increases in Inflammation. Blood 113: 5202-5205.
Dixit VD. (2008) Hormonal, neural, and metabolic regulation of immunity. J Leukoc Biol. 84: 881. (Editorial for JLB special issue)
Dixit VD. (2008) Adipose-Immune interactions during obesity and caloric restriction: reciprocal mechanisms regulating immunity and health span. J Leukoc Biol. 84: 821-892. (Featured Article for JLB Cover Page)
Yang H, Dixit VD, Patel K, Vandanmagsar B, Collins G, Sun Y, Smith RG, Taub D. (2008). Reduction in hypophyseal growth hormone and prolactin expression due to deficiency in ghrelin receptor signaling is associated with Pit-1 suppression: Relevance to the immune system. Brain Behav Immun. 2008 Jun 17. [Epub ahead of print]
Yang H, Youm YH, Nakata C and Dixit VD. (2007) Chronic Caloric Restriction Induces Forestomach Hypertrophy with Enhanced Ghrelin Levels During Aging. Peptides. 10: 1931-1936.
Dixit VD, Yang H, Sun Y, Youm YH, Weeraratna AT, et al. (2007). Ghrelin promotes thymopoiesis during aging. J. Clin. Invest. 117: 2778-2790.
* Article Selected as Editors Highlight in JCI.
Giri B, Dixit VD, Ghosh M, Collinns GD, Khan IU, Madara K, Weeraratna AT and Taub DD. (2007) CXCL12-induced partitioning of flotillin-1 with lipid-rafts plays a role in CXCR4 function. Eur. J. Immunol. 37: 2104-2116.
*Article selected as cover image of EJI.
Johnson JB, Summer W, Cutler RG, Martin B, Hyun DH, Dixit VD, Pearson M, Nassar M, Tellejohan R, Maudsley S, Carlson O, John S, Laub DR, Mattson MP. (2007). Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma. Free Radic Biol Med. 42: 665-74
Dixit VD, Weeraratna AT, Yang H, Bertak, D, Cooper-Jenkins A, Riggins GJ, Eberhart C, Taub DD. (2006) Ghrelin and growth hormone secretagogue receptor constitute a novel autocrine pathway in astrocytoma motility. J. Biol. Chem. 281: 16681-16690.
Dawson HD, Collins G, Pyle R, Key M, Weeraratna A, Dixit VD, Nadal CV and Dennis D Taub. (2006)Direct and Indirect Effects of Retinoic Acid on Human Th2 Cytokine and Chemokine Expression by Human T Lymphocytes. BMC Immunology. 7: 27.
Arumugam TV, Chan SL, Yilmaz G, Jo DG, Tang SC, Gleichmann M, Cheng A, Okun A, Dixit VD, Xin O, Miele L, Magnus T, Granger DN and Mattson MP (2006). Gamma Secretase-Mediated Notch Signaling Worsens Brain Damage and Functional Outcome in Ischemic Stroke. Nat. Med. 12(6):621-623.
Ruggiero C, Cherubini A, Ble A, Bos AJ, Maggio M, Dixit VD, Lauretani F, Bandinelli S, Senin U, Ferrucci L. (2006). Uric Acid and Inflammatory Markers. European Heart J. 27: 1174-1181.
Dixit VD and Taub D. (2005) Ghrelin and Immunity: A Young Player in an Old Field. Exp. Geron. 40: 900-910.
Dixit VD, Schaffer EM, Pyle RS, Collins GD, Sakthivel SK, Palaniappan R, Lillard Jr JW and Taub DD. (2004). Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells. *J Clin. Invest. 114: 57-66.
*Article selected as Highlight in July 1st 2004 issue of J. Clin Invest.
*Article selected for commentary in Science SAGE KE, July 14th 2004.
Hu L, Dixit VD, Coelho V, Taub DD. (2004). Age-associated alterations in CXCL1 chemokine expression by murine B cells. BMC Immunology 5: 15.
Dawson H, Collins G, Pyle RS, Dixit VD, Taub D. (2004). The immunoregulatory effect of homocysteine and its intermediates on T-lymphocyte function. Mech. Ageing Dev. 125: 107-110.
Nagel JE, Smith RJ, Shaw L, Bertak D, Dixit VD, Schaffer EM, Taub DD. (2004) Identification of genes differentially expressed in T cells following stimulation with the chemokines CXCL12 and CXCL10. BMC Immunology. 5: 17.
Dixit VD., Mielenz M, Taub DD, Parvizi N. (2003). Leptin Induces Growth Hormone Secretion From Peripheral Blood Mononuclear Cells Via a Protein Kinase C and Nitric oxide Dependent Mechanisms. Endocrinology, 144: 5595-5603.
Dixit VD, Sridaran R, Edmonsond MJ, Taub D, Thompson WE. (2003). Gonadotropin releasing hormone attenuates pregnancy-associated thymic involution and modulates expression of anti-proliferative gene product prohibitin. Endocrinology 144: 1496-14505.
Dixit VD, Yang H, Udhayakumar V, Sridaran R. (2003). Gonadotropin releasing hormone alters T helper cytokine balance in pregnant rat. Biol. Reprod. 68: 2215-2221.
Poppi L., Dixit VD., Baratta M., Giustina A., Tamanini C., and Parvizi N. (2002). Growth hormone secretagogue analogue Hexarelin stimulates GH secretion from lymphocytes. Exp. Clin Endocrinol Diabetes. 110: 343-347.
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