Dr. Barbara Lee-Faubert Kaplan |
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Michigan State University College of Veterinary Medicine Center for Integrative Toxicology Assistant ProfessorAppointed: 2004 |
Mailing Address313 Food Safety and Toxicology East Lansing, Michigan 48824United States | Contact Information |
Qualifications
Ph.D., Michigan State University, Pharmacology and Toxicology, 2001.
B.S., University of California, Davis, Environmental Toxiocology, 1992.
Expertise and Research Interests
The focus of my research is to understand the mechanism by which cannabinoid compounds modulate T cell function. Plant-derived cannabinoid compounds (i.e., those derived from marijuana) include both psychoactive (such as delta-9-tetrahydrocannabinol) and non-psychoactive (such as cannabinol and cannabidiol) compounds. The ability of these compounds to exhibit psychoactive properties correlates with their binding affinity to one of the cloned cannabinoid receptors, CB1. Despite differences in cannabinoid receptor binding affinity and magnitude of psychoactive properties, many of the plant-derived cannabinoid compounds possess immunomodulatory actions.
I am currently focusing on two projects.
First, I am characterizing the mechanisms by which cannabidiol, a non-psychoactive plant-derived cannabinoid, modulates immune function. Cannabidiol will either suppress or stimulate cytokine production (IL-2, IFN-gamma) depending on the magnitude of lymphocyte activation. Interestingly, cannabidiol, in the absence of activation, increases intracellular calcium. The intracellular targets of cannabidiol and lymphocyte activation are being investigated.
Second, I am determining the effect of two plant-derived cannabinoids, cannabidiol and delta-9-tetrahydrocannabinol, on pulmonary inflammation. Cannabinoid compounds have been described as anti-inflammatory, yet there are instances in which they possess modest stimulatory effects on inflammatory mediators.
I am currently focusing on two projects.
First, I am characterizing the mechanisms by which cannabidiol, a non-psychoactive plant-derived cannabinoid, modulates immune function. Cannabidiol will either suppress or stimulate cytokine production (IL-2, IFN-gamma) depending on the magnitude of lymphocyte activation. Interestingly, cannabidiol, in the absence of activation, increases intracellular calcium. The intracellular targets of cannabidiol and lymphocyte activation are being investigated.
Second, I am determining the effect of two plant-derived cannabinoids, cannabidiol and delta-9-tetrahydrocannabinol, on pulmonary inflammation. Cannabinoid compounds have been described as anti-inflammatory, yet there are instances in which they possess modest stimulatory effects on inflammatory mediators.
Future Research
Future projects will focus on the effect of cannabinoids on neuroimmune interactions. Cannabinoid compounds are unique in that they have been shown to modulate neuronal activity in the CNS and produce immune suppression. The main focus of my future research will be address the role of neuroimmune interactions in cannabinoid-induced immune suppression.
Keywords
COS Keywords:
Immunology, Toxicology.Additional Terms:
Immunology, Immunotoxicology.Languages
(Reading, Writing, Speaking)
English: (Fluent, Fluent, Fluent)
Memberships
Society of Neuroimmune Pharmacology
Society of Toxicology
Honors and Awards
2008, Intramural Seed Grant,
Michigan State University Respiratory Research Initiative Group
2007,
Junior Faculty Travel Award for Immunology, 2007,
American Association of Immunology
2006,
Intramural Seed Grant,
Michigan State University Respiratory Research Initiative Group
2006,
Research Expense Award,
Michigan State University National Food Safety and Toxicology Center
Previous Positions
2001-2004, Research Associate,
University of Chicago,
Surgery
1994-1995, Chemist III,
Quanterra, Inc.
1992-1994, Chemist I,
Eureka Laboratories, Inc.
Funding Received
- National Institute of Environmental Health Sciences: Environmental, Microbial and Mammalian Biomolecular Responses to AhR Ligands, Co-investigator, 2006 to 2011.
- National Institute on Drug Abuse: IL-2 Suppression by Endocannabinoid Activation of PPAR-gamma, Co-investigator, 2005 to 2010.
Publications
- Lu H, Kaplan BL, Ngaotepprutaram T, Kaminski NE (Nov 2008) Suppression of T cell costimulator ICOS by {Delta}9-tetrahydrocannabinol., Journal of leukocyte biology, 85 (2), 322-29
- Springs AE, Karmaus PW, Crawford RB, Kaplan BL, Kaminski NE (Dec 2008) Effects of targeted deletion of cannabinoid receptors CB1 and CB2 on immune competence and sensitivity to immune modulation by {Delta}9-tetrahydrocannabinol., Journal of leukocyte biology, 84 (6), 1574-84
- Kaplan BL, Springs AE, Kaminski NE (Sep 2008) The profile of immune modulation by cannabidiol (CBD) involves deregulation of nuclear factor of activated T cells (NFAT)., Biochemical pharmacology, 76 (6), 726-37
- Rockwell CE, Raman P, Kaplan BL, Kaminski NE (Aug 2008) A COX-2 metabolite of the endogenous cannabinoid, 2-arachidonyl glycerol, mediates suppression of IL-2 secretion in activated Jurkat T cells., Biochemical pharmacology, 76 (3), 353-61
- Kaminski NE, Kaplan BL, Holsapple MP (2007) Toxic Responses of the Immune System In Klaassen CD (eds), Casarett and Doull's Toxicology, 7th Edition, New York, McGraw Hill (bookchapter)
- Kaplan BL, Callender GG, Norell H, Kiessling R, Nishimura MI (Jun 2006) Interferon-gamma renders tumors that express low levels of Her-2/neu sensitive to cytotoxic T cells., Cancer Immunol Immunother, 55 (6), 653-62
- Kaplan BL, Ouyang Y, Herring A, Yea SS, Razdan R, Kaminski NE (Jun 2005) Inhibition of leukocyte function and interleukin-2 gene expression by
2-methylarachidonyl-(2'-fluoroethyl)amide, a stable congener of the
endogenous cannabinoid receptor ligand anandamide., Toxicology and Applied Pharmacology, 205 (2), 107-15
- Kaplan BL, Moore TV, Schreiber K, Callender GG, Schreiber H, Nishimura MI (Jun 2005) A new murine tumor model for studying HLA-A2-restricted anti-tumor
immunity., Cancer Letters, 224 (1), 153-66
- Kaplan BL, Ouyang Y, Rockwell CE, Rao GK, Kaminski NE (Jun 2005) 2-Arachidonoyl-glycerol suppresses interferon-gamma production in phorbol
ester/ionomycin-activated mouse splenocytes independent of CB1 or
CB2., Journal of Leukocyte Biology, 77 (6), 966-74
- Faubert Kaplan BL, Kaminski NE (Oct 2003) Cannabinoids inhibit the activation of ERK MAPK in PMA/Io-stimulated mouse
splenocytes., International Immunopharmacology, 3 (10-11), 1503-10
- Kaplan BL, Rockwell CE, Kaminski NE (Sep 2003) Evidence for cannabinoid receptor-dependent and -independent mechanisms of
action in leukocytes., The Journal of Pharmacology and Experimental Therapeutics, 306 (3), 1077-85
- Kaplan BL, Yu DC, Clay TM, Nishimura MI (May-Aug 2003) Redirecting T lymphocyte specificity using T cell receptor genes., International Reviews of Immunology, 22 (3-4), 229-53
- Herring AC, Faubert Kaplan BL, Kaminski NE (Apr 2001) Modulation of CREB and NF-kappaB signal transduction by cannabinol in
activated thymocytes., Cellular Signalling, 13 (4), 241-50
- Faubert BL, Kaminski NE (Feb 2000) AP-1 activity is negatively regulated by cannabinol through inhibition of
its protein components, c-fos and c-jun., Journal of Leukocyte Biology, 67 (2), 259-66
Profile Details
Last Updated: 5/20/2009
COS Expertise ID #1227468
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