Dr. Josep Bassaganya-Riera |
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Virginia Polytechnic Institute and State University Virginia Bioinformatics Institute Nutritional Immunology & Molecular Nutrition Laboratory Associate ProfessorAppointed: 2008 |  |
Mailing AddressNutritional Immunology & Molecular Nutrition Lab 363E Virginia Bioinformatics Institute Washington Street (0477) http://www.vbi.vt.edu/nutritional_immunology Blacksburg, Virginia 24061-0430United States | Contact InformationPhone: (540) 231-7421 Fax: (540) 231-2606 jbassaga@vt.edu or jbassaga@vbi.vt.edu https://www.vbi.vt.edu/faculty/personal_pages/josep_bassaganya-riera |
Qualifications
Ph.D., Iowa State University, Nutrition and Immunology, 2000.
D.V.M., Autonomous University of Barcelona, Veterinary Medicine, 1997.
Expertise and Research Interests
The long-term goal of my laboratory is to elucidate the cellular and molecular mechanism(s) by which dietary lipids and phytochemicals regulate homeostasis and prevent chronic diseases. In line with this long-term goal, three lines of research are currently ongoing in my laboratory: 1) nutritional immunology, 2) gastrointestinal health and 3) obesity and its comorbidities (i.e., type 2 diabetes and cardiovascular disease). Modulation of inflammation and immune function are common integrative themes.
Nutritional Immunology: My initial research characterized the modulatory effects of dietary lipids on the induction of effector T cell responses to bacterial and viral pathogens. This line of research originated when I first demonstrated that dietary conjugated linoleic acid (CLA)-supplementation enhanced numbers of CD8+ peripheral blood lymphocytes. CLA is a mixture of positional and geometric isomers of octadecadienoic acid with conjugated double bonds. Our central hypothesis was that CLA exerted its immunomodulatory effects by modulating the activity of several subsets of CD8+ T cells. This research, which helped establish the links between nutrition and immunology was recently recognized by the American Society of Nutritional Sciences from which I was awarded the 2005 Bio-Serv Award in Experimental Animal Nutrition. Also related to my nutritional immunology program, in August of 2004, I was awarded $263,439 by Mead Johnson Nutritionals-Bristol Myers Squibb for the project entitled "Assessment of a docosahexaenoic acid (DHA) and arachidonic acid (ARA)-enriched infant formula on immune responses in neonatal piglets." We found that when DHA and ARA are fed in combination (0.63/0.34%) to neonatal piglets they elicit significant immunosuppressive effects. These results raise questions about the safety of adding these two fatty acids in infant formulas. Infant formulas are the only source of nutrition for many infants during the first 4 to 6 months of life. The minimum concentrations of 29 nutrients are tightly regulated in the U.S. and worldwide. Thus, investigating the effects of new infant formula ingredients on immune function of infants and neonates represents an important public health issue. The pig is the best model for evaluating the efficacy and safety of new ingredients.
Gastrointestinal Health: Peroxisome proliferator-activated receptors (PPARs) are novel members of the nuclear receptor superfamily with three isoforms (alpha, gamma, and delta) that translate nutritional or pharmacologic stimuli into changes in gene expression. Originally, PPARs were identified as components of adipocyte gene expression and differentiation. More recent data suggest a central role for PPARs in regulating inflammation and immune function. The two clinical manifestations of inflammatory bowel disease (IBD) -- Crohn's disease (CD) and ulcerative colitis (UC) -- afflict over 1 million people in North America and 4 million people worldwide. Current treatments against IBD have improved, but they are modestly successful for the long-term management of the disease and result in significant side effects. The basic understanding of the mechanisms by which dietary compounds and their endogenous metabolites prevent mucosal inflammation is directly relevant to CD, UC, celiac disease, inflammation-induced colorectal cancer and to gastrointestinal infection caused by pathogens and indirectly relevant to type 1 diabetes. I first reported the efficacy of CLA in ameliorating gut inflammation in a pig model and proposed that some of the beneficial effects of CLA on mucosal immune responses could be mediated by epithelial and immune cell PPAR gamma. Recent results fulfilled the prediction of our previous hypothesis, as the deletion of the PPAR ? gene in immune and epithelial cells abrogated CLA's anti-inflammatory actions in the gut. This work was published in Gastroenterology. I have put considerable effort into further dissecting the PPAR gamma- and delta-dependent mechanism(s) of action of dietary lipids and endogenous agonists. We are currently investigating whether endogenous PPAR gamma activation is required for the function of regulatory T cells (Treg) - important negative regulators of inflammatory and autoimmune responses. In May of 2006, I was awarded the Junior Faculty Travel Award by the American Association of Immunologists for presenting our Treg work. We found that PPAR gamma is required for Treg's anti-inflammatory function. Consistent with the concept from bench to bedside, I am translating the basic scientific understanding of the role of PPAR gamma in the pathophysiology of gut inflammation into the clinic through extramurally funded research collaborations with Wake Forest University and the Digestive Health Center of Excellence at University of Virginia.
Type 2 Diabetes and Obesity: According to recent estimates from the Centers for Disease Control, 30% of the U.S. population is obese and 65% is overweight. One of the major consequences of these high rates is manifested by the increased prevalence of Type 2 Diabetes Mellitus (T2D), a chronic disease characterized by systemic insulin resistance and inflammation. In 2004, it was estimated that 20.8 million Americans had T2D and over 40.1% of middle-aged adults have prediabetes, with healthcare costs for diabetes treatment over $132 billion and $394 billion for treating cardiovascular disease and stroke. Current antidiabetic drugs elicit important insulin-sensitizing and anti-inflammatory effects, but side effects associated with using these medications are significant. Our laboratory is actively screening and discovering novel, naturally occurring, orally active nutraceuticals against diabetes and CVD that activate nuclear receptors. Of note is the discovery of a PPAR gamma-activating and anti-inflammatory phytohormone, abscisic acid (ABA), which is also a potent antidiabetic agent. Following an in vitro screening of its PPAR gamma agonistic activity, we generated molecular evidence in vivo showing that ABA improves insulin sensitivity and obesity-related inflammation by inhibiting monocyte chemoattractant-1 (MCP-1) expression and macrophage infiltration through a PPAR gamma-dependent mechanism. We plan to use ABA as a proof-of-concept to establish a solid innovation pipeline of immune modulatory compounds for chronic disease prevention. This line of research builds upon my expertise in inflammation, immunity and nuclear receptor biology (i.e., PPAR gamma). This research provides an opportunity for expanding our laboratory's efforts into a botanical center.
Nutritional Immunology: My initial research characterized the modulatory effects of dietary lipids on the induction of effector T cell responses to bacterial and viral pathogens. This line of research originated when I first demonstrated that dietary conjugated linoleic acid (CLA)-supplementation enhanced numbers of CD8+ peripheral blood lymphocytes. CLA is a mixture of positional and geometric isomers of octadecadienoic acid with conjugated double bonds. Our central hypothesis was that CLA exerted its immunomodulatory effects by modulating the activity of several subsets of CD8+ T cells. This research, which helped establish the links between nutrition and immunology was recently recognized by the American Society of Nutritional Sciences from which I was awarded the 2005 Bio-Serv Award in Experimental Animal Nutrition. Also related to my nutritional immunology program, in August of 2004, I was awarded $263,439 by Mead Johnson Nutritionals-Bristol Myers Squibb for the project entitled "Assessment of a docosahexaenoic acid (DHA) and arachidonic acid (ARA)-enriched infant formula on immune responses in neonatal piglets." We found that when DHA and ARA are fed in combination (0.63/0.34%) to neonatal piglets they elicit significant immunosuppressive effects. These results raise questions about the safety of adding these two fatty acids in infant formulas. Infant formulas are the only source of nutrition for many infants during the first 4 to 6 months of life. The minimum concentrations of 29 nutrients are tightly regulated in the U.S. and worldwide. Thus, investigating the effects of new infant formula ingredients on immune function of infants and neonates represents an important public health issue. The pig is the best model for evaluating the efficacy and safety of new ingredients.
Gastrointestinal Health: Peroxisome proliferator-activated receptors (PPARs) are novel members of the nuclear receptor superfamily with three isoforms (alpha, gamma, and delta) that translate nutritional or pharmacologic stimuli into changes in gene expression. Originally, PPARs were identified as components of adipocyte gene expression and differentiation. More recent data suggest a central role for PPARs in regulating inflammation and immune function. The two clinical manifestations of inflammatory bowel disease (IBD) -- Crohn's disease (CD) and ulcerative colitis (UC) -- afflict over 1 million people in North America and 4 million people worldwide. Current treatments against IBD have improved, but they are modestly successful for the long-term management of the disease and result in significant side effects. The basic understanding of the mechanisms by which dietary compounds and their endogenous metabolites prevent mucosal inflammation is directly relevant to CD, UC, celiac disease, inflammation-induced colorectal cancer and to gastrointestinal infection caused by pathogens and indirectly relevant to type 1 diabetes. I first reported the efficacy of CLA in ameliorating gut inflammation in a pig model and proposed that some of the beneficial effects of CLA on mucosal immune responses could be mediated by epithelial and immune cell PPAR gamma. Recent results fulfilled the prediction of our previous hypothesis, as the deletion of the PPAR ? gene in immune and epithelial cells abrogated CLA's anti-inflammatory actions in the gut. This work was published in Gastroenterology. I have put considerable effort into further dissecting the PPAR gamma- and delta-dependent mechanism(s) of action of dietary lipids and endogenous agonists. We are currently investigating whether endogenous PPAR gamma activation is required for the function of regulatory T cells (Treg) - important negative regulators of inflammatory and autoimmune responses. In May of 2006, I was awarded the Junior Faculty Travel Award by the American Association of Immunologists for presenting our Treg work. We found that PPAR gamma is required for Treg's anti-inflammatory function. Consistent with the concept from bench to bedside, I am translating the basic scientific understanding of the role of PPAR gamma in the pathophysiology of gut inflammation into the clinic through extramurally funded research collaborations with Wake Forest University and the Digestive Health Center of Excellence at University of Virginia.
Type 2 Diabetes and Obesity: According to recent estimates from the Centers for Disease Control, 30% of the U.S. population is obese and 65% is overweight. One of the major consequences of these high rates is manifested by the increased prevalence of Type 2 Diabetes Mellitus (T2D), a chronic disease characterized by systemic insulin resistance and inflammation. In 2004, it was estimated that 20.8 million Americans had T2D and over 40.1% of middle-aged adults have prediabetes, with healthcare costs for diabetes treatment over $132 billion and $394 billion for treating cardiovascular disease and stroke. Current antidiabetic drugs elicit important insulin-sensitizing and anti-inflammatory effects, but side effects associated with using these medications are significant. Our laboratory is actively screening and discovering novel, naturally occurring, orally active nutraceuticals against diabetes and CVD that activate nuclear receptors. Of note is the discovery of a PPAR gamma-activating and anti-inflammatory phytohormone, abscisic acid (ABA), which is also a potent antidiabetic agent. Following an in vitro screening of its PPAR gamma agonistic activity, we generated molecular evidence in vivo showing that ABA improves insulin sensitivity and obesity-related inflammation by inhibiting monocyte chemoattractant-1 (MCP-1) expression and macrophage infiltration through a PPAR gamma-dependent mechanism. We plan to use ABA as a proof-of-concept to establish a solid innovation pipeline of immune modulatory compounds for chronic disease prevention. This line of research builds upon my expertise in inflammation, immunity and nuclear receptor biology (i.e., PPAR gamma). This research provides an opportunity for expanding our laboratory's efforts into a botanical center.
Keywords
COS Keywords:
Animal Science, Exercise, Gastroenterology, Gene Expression, Immunology, Inflammatory Bowel Disease, Nutrition or Dietetics, Veterinary Medicine.Additional Terms:
Conjugated Linoleic Acid, Infant Formula, Inflammatory Bowel Disease, Molecular Nutrition, Nutrition Immunology.Languages
(Reading, Writing, Speaking)
Catalan-Valencian-Balear: (Fluent, Fluent, Fluent)
English: (Fluent, Fluent, Fluent)
Spanish: (Fluent, Fluent, Fluent)
French: (Fluent, Fluent, Functional)
Memberships
American Association of Immunologists
American Gastroenterological Association
American Oil Chemists' Society
American Society for Nutritional Sciences
American Society of Animal Science
Federation of American Societies for Experimental Biology
Honors and Awards
2006, AAI Travel Award,
American Association of Immunologists
2005, Bio-Serv Award in Experimental Animal Nutrition,
American Society for Nutritional Sciences
2000, Research Excellence Award,
Iowa State University
1999, Gamma Sigma Delta,
Honor Society of Agriculture,
Iowa State University
Previous Positions
2003-2007, Assistant Professor,
Virginia Polytechnic Institute and State University,
College of Agriculture and Life Sciences,
Human Nutrition, Foods and Exercise,
Nutritional Immunology & Molecular Nutrition Laboratory
2001-2002, Associate Scientist,
Iowa State University,
Veterinary Medical Research Institute,
Nutritional Immunology and Molecular Nutrition Laboratory
2000-2001, Assistant Scientist,
Iowa State University
Research Assistant,
Iowa State University,
Animal Sciences
Patents
A method of treating and/or preventing type 2 diabetes and related disorders,
Patent Number: ,
2007,
Institution,
United States of America.
Method of using probiotic bacteria to prevent insulin resistance and obesity-related inflammation,
Patent Number: ,
2007,
Institution,
United States of America.
Funding Received
- National Institutes of Health (NIH): Mechanisms of immune modulation by abscisic acid, $1,234,000, 2007 to 2011.
- Cognis Nutrition & Health: Nutritional regulation of Crohn's Disease by CLA, $316,000, 2006 to 2008.
- Institute for Biomedical and Public Health Sciences: Molecular targets of abscisic acid in obesity-related inflammation, $30,000, 2006 to .
- ASPIRES-Virginia Tech.: Molecular Targets for Genistein in Vascular Endothelial Cells, $115,904, 2004 to 2005.
- Mead Johnson Nutritionals/BMS: Assessment of a DHA/AA-Enriched Infant Formula on Immune Response and Function in Piglets, $360,000, 2004 to 2005.
- Center for Designing Foods to Improve Nutrition-United States Department of Agriculture: Nutritional regulation of viral disease, $32,518, 2002 to 2003.
- National Pork Board: Defining the Health Benefits of the Nutritional Interaction between conjugated linoleic acid and (n-3) fatty acids.”, $50,000, 2002 to 2003.
- Iowa Pork Producers Association: Development of a Nutritional Therapy Against the Post-Weaning Multisystemic Wasting Syndrome, $17,058, 2001 to 2002.
- National Pork Board: Conjugated Linoleic Acid: a dietary Immune Modulator that Decreases Intestinal Inflammation, $47,941, 2001 to 2002.
- Immunology Competitive Grants Program: Microdissection of the Colonic Mucosa, $9,000, 2001 to 2002.
- National Pork Board: Ability of CLA to Improve the Efficacy of a Dysentery Vaccine, $25,000, 2000 to 2001.
- USDA-NRI: Immunoregulation of Bacterial-induced Colitis, $180,000, 2000 to 2003.
Publications
- Thakare, K, Shi, W, Barbeau, WE, Bassaganya-Riera, J, Hontecillas, R, Scott, F (2008) Investigation of chloroform-methanol soluble wheat proteins and sphingolipids as potential dietary triggers of diabetes in BBdp rats., Food and Agricultural Immunology, In Press
- A.J. Guri, Hontecillas, R, Bassaganya-Riera, J (2008) Dietary modulators of PPARs: Implications for the prevention and treatment of metabolic syndrome., Nutrigenetics and Nutrigenomics, In Press
- A.J. Guri, Hontecillas, R, Ferrer, G, Casagran, O, Wankahade, U, Noble, AM, Eizirik, DL, Ortis, F, Cnop, M, Liu, D, Si, H, Bassaganya-Riera, J (2007) Loss of PPARgamma in immune cells impairs the ability of abscisic acid to improve insulin sensitivity by suppressing monocyte chemoattractant protein-1 expression and macrophage infiltration into white adipose tissue., Journal of Nutritional Biochemistry, In Press
- Hontecillas, R, Bassaganya-Riera, J (2007) Peroxisome proliferator-activated receptor gamma is required for regulatory CD4+ T cell-mediated protection against colitis., Journal of Immunology, 178 (5), 2940-2949
- Bassaganya-Riera, J, King, J, Noble, AM, Reynolds, KA, Reynolds, K, Wood, CM, Ashby, M, Rai, D, Hontecillas, R (2007) Docosahexaenoic and arachidonic acid-enriched infant formulas modulate antigen-specific T cell responses in the neonate, American Journal of Clinical Nutrition, 85 (3), 824-836
- Bassaganya-Riera, J, Hontecillas, R (2006) CLA and n-3 PUFA differentially modulate clinical activity and colonic PPAR-responsive gene expression in a pig model of experimental IBD, Clinical Nutrition, 25, 454-465
- Barbeau, W, Bassaganya-Riera, J, Hontecillas, R (2007) Putting the pieces of the puzzle together: A series of hypotheses on the etiology and pathogenesis of type 1 diabetes, Medical Hypotheses, 68 (3), 607-619
- Guri, A, Hontecillas, R, Si, H, Liu, D, Bassaganya-Riera, J (2006) Dietary abscisic acid ameliorates glucose tolerance and obesity-related inflammation in db/db mice fed high-fat diets, Clinical Nutrition, 26 (1), 107-116
- Guri, A, Hontecillas, R, Bassaganya-Riera, J (2006) Peroxisome Proliferator-Activated Receptors: bridging metabolic syndrome through molecular nutrition, Clinical Nutrition, 25 (6), 871-885
- Hontecillas R, Bassaganya-Riera J, Wilson J, Hutto DL, Wannemuehler MJ (May 2005) CD4+ T-cell responses and distribution at the colonic mucosa during
Brachyspira hyodysenteriae-induced colitis in pigs., Immunology, 115 (1), 127-35
- Bassaganya-Riera, J, Guri, A, King, J, Hontecillas, R, Peroxisome Proliferator-Activated Receptors: the Nutritionally Controlled Molecular Networks That Integrate Inflammation, Immunity and Metabolism., Current Nutrition and Food Science, 1, 179-187, 2005
- Bassaganya-Riera J, Reynolds K, Martino-Catt S, Cui Y, Hennighausen L, Gonzalez F, Rohrer J, Benninghoff AU, Hontecillas R, Activation of PPAR Gamma and Delta By Conjugated Linoleic Acid Mediates Protection From Experimental Inflammatory Bowel Disease., Gastroenterology, 127(3), 777-91, Sep 2004
- O'Shea M, Bassaganya-Riera J, Mohede IC, Immunomodulatory properties of conjugated linoleic acid, The American Journal of Clinical Nutrition, 79(6 Suppl), 1199S-1206S, 2004
- Bassaganya-Riera J, Thacker BJ, Yu S, Strait E, Wannemuehler MJ, Thacker EL, Impact of immunizations with porcine reproductive and respiratory syndrome
virus on lymphoproliferative recall responses of CD8+ T
cells, Viral Immunology, 17(1), 25-37, 2004
- Bassaganya-Riera, J., J. King, and R. Ho, Health Benefits of CLA: Lessons From Pig Models in Biomedical Research, European Journal of Lipid Science and Technology, 106, 856-861, 2004
- Bassaganya-Riera J, Pogranichniy RM, Jobgen SC, Halbur PG, Yoon KJ, O'Shea M, Mohede I, Hontecillas R, Conjugated linoleic acid ameliorates viral infectivity in a pig model of
virally induced immunosuppression, The Journal of Nutrition, 133(10), 3204-14, 2003
- Hontecillas R, Bassaganya-Riera J, Differential requirements for proliferation of CD4+ and gammadelta+ T
cells to spirochetal antigens, Cellular Immunology, 224(1), 38-46, 2003
- Bassaganya-Riera J, Hontecillas R, Beitz DC, Colonic anti-inflammatory mechanisms of conjugated linoleic acid, Clinical Nutrition (edinburgh, Lothian), 21(6), 451-9, 2002
- Hontecillas R, Wannemeulher MJ, Zimmerman DR, Hutto DL, Wilson JH, Ahn DU, Bassaganya-Riera J, Nutritional regulation of porcine bacterial-induced colitis by conjugated
linoleic acid, The Journal of Nutrition, 132(7), 2019-27, 2002
- Bassaganya-Riera J, Hontecillas R, Zimmerman DR, Wannemuehler MJ, Long-term influence of lipid nutrition on the induction of CD8(+)
responses to viral or bacterial antigens, Vaccine, 20(9-10), 1435-44, 2002
- Bassaganya-Riera, J., R. Hontecillas, and, M. J. Wannemuehler., Nutritional impact of conjugated linoleic acid: a model functional food ingredient, In Vitro Cellular and Developmental Biology, 38(3), 241-246, 2002
- Bassaganya-Riera J, Hontecillas R, Zimmerman DR, Wannemuehler MJ, Dietary conjugated linoleic acid modulates phenotype and effector
functions of porcine CD8(+) lymphocytes, The Journal of Nutrition, 131(9), 2370-7, 2001
- Bassaganya-Riera J, Hontecillas-Magarzo R, Bregendahl K, Wannemuehler MJ, Zimmerman DR, Effects of dietary conjugated linoleic acid in nursery pigs of dirty and
clean environments on growth, empty body composition, and immune
competence, Journal of Animal Science, 79(3), 714-21, 2001
- Waters WR, Hontecillas R, Sacco RE, Zuckermann FA, Harkins KR, Bassaganya-Riera J, Wannemuehler MJ, Antigen-specific proliferation of porcine CD8alphaalpha cells to an
extracellular bacterial pathogen, Immunology, 101(3), 333-41, 2000
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