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Arkansas Center for Environmental Exposure Research (ACEER)

Our mission is to dimish the impact of pollutants on human health and the enviromnent.

ACEER was initiated using funds from the Arkansas Biosciences Institute (ABI), the major research component of the Tobacco Settlement Proceeds Act of 2000.

ACEER was established in 2002 at the Arkansas Children's Hospital Research Institute in Little Rock, Arkansas. Since then, ACEER has fostered key collaborations across the state and nation with researchers at institutions including Arkansas State University in Jonesboro, the University of Arkansas for Medical Sciences in Little Rock, the University of Central Arkansas in Conway, and Colorado State University in Fort Collins.

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Dr. GilbertKathleen Gilbert, Ph.D., Center Director, Professor of Microbiology and Immunology

Research Focus: TCE-induced autoimmune disease

Dr. Kathleen Gilbert and her team of researchers at ACEER are examining how exposure to common environmental toxicants triggers autoimmune disease. Her research is focused on how chronic low-level exposure to trichloroethylene alone, or in mixtures with other chemicals such as mercury, affects immune cells and promotes autoimmune disease. Immune responses typically protect the body from infectious diseases. When the immune response instead targets its own tissues, autoimmune diseases such as lupus, scleroderma, alopecia, and autoimmune hepatitis can occur. Various interacting factors are required for disease development. Although genetics plays a role in autoimmunity, there is evidence that the environmental influence, such as exposure to toxicants, is equally important. Typically, unsafe levels of a toxicant are determined by whether a concentration causes cancer. At lower levels that are not carcinogenic, the chemicals can still impact human health by promoting autoimmune disease. Evaluating the mechanisms by which low-level exposure to pollutants, such as trichloroethylene, promote autoimmune diseases will help identify interventions. Dr. Gilbert's work has started to encompass toxicant-induced epigenetic changes; i.e., long-term alterations in gene expression that can have extended effects on immune cell function. This could help explain how developmental or early life exposure to certain chemicals can increase risk of adult disease.

Click Here to View Dr. Gilbert's Publications
  • Gilbert, K.M., Nelson, A.R, Cooney, C.A., Reisfeld, B., and Blossom, S.J. Epigenetic alterations may regulate temporary reversal of CD4+ T cell activation caused by trichloroethylene exposure. Toxicological Sciences. 2012 May;127(1):169-78. Epub 2012 Mar 9.
  • Blossom S.J., Melnyk, S., Cooney C.A., Gilbert K.M., and James, S.J. Postnatal exposure to trichloroethylene alters glutathione redox homeostasis, methylation potential, and neurotrophin expression in the mouse hippocampus. Neurotoxicology. Mar 7, 2012 [Epub ahead of print].
  • Cooney, C.A., and Gilbert, K.M. Toxicology, Epigenetics and Autoimmunity in Toxicology and Epigenetics, Edited by Saura C. Sahu. Wiley-Blackwell Inc. In Press.
  • Gilbert, K.M.  Toxicant-induced Autoimmune Hepatitis.  Hepatitis Research and Treatment, 2010:248157, 2010.
  • Gilbert, K.M., Rowley, B., Gomez-Acevedo, H., and Blossom, S.J. Co-exposure to mercury increases immunotoxicity of trichloroethylene. Toxicological Sciences, 119:281-292, 2011.
  • Gilbert, K.M., Przybyla, B., Pumford, N.R., Han, T, Fuscoe, J., Schnackenberg, L.K., Holland, R.D., Doss, J.C. MacMillan-Crow, L, and Blossom, S.J. Delineating liver events in trichloroethylene-induced autoimmune hepatitis, Chemical Research in Toxicology  22: 623-632, 2009.
  • Gilbert, K.M., Blossom, S.J., and Pumford, N.  Comments on “Lifetime exposure to trichloroethylene (TCE) does not accelerate autoimmune disease in MRL+/+ mice, Journal of Environmental Health Sciences, Part A,  44:116, 2009.
  • Cooper, G.S., Gilbert, K.M., Greidinger, E.L, James, J.A., Pfau, J.C., Reinlib, L., Richardson, B.C., and Rose, N.R.  Recent advances and opportunities in research on lupus: Environmental Influences and Mechanisms of Disease, Environmental Health Perspectives 116: d Gilbert, K.M.  Chronic exposure to a trichloroethylene metabolite i695–702, 2008
  • Blossom, S.J., Doss, J.C. an n autoimmune-prone MRL+/+ mice promotes immune modulation and alopecia.  Toxicological Sciences 95(2):401-11, 2007.
  • Gilbert, K.M. and Luebke, R. Overview of Platform Session “Immunotoxicology”: Society of Toxicology 45th Annual Meeting, Journal of Immunotoxicology, 3: 213-216, 2006.
  • Gilbert, K.M., Pumford, N., and Blossom, S.J.  Environmental contaminant trichloroethylene promotes autoimmune disease and inhibits T cell apoptosis in MRL+/+ mice.  Journal of Immunotoxicology 3:263-267, 2006.
  • Blossom, S.J. and Gilbert, K.M.  Ability of environmental toxicant trichloroethylene to promote immune pathology is strain-specific.  Journal of Immunotoxicology 3:179-188, 2006.
  • Blossom, S.J., and Gilbert, K.M.  Exposure to a metabolite of the environmental toxicant, trichloroethylene attenuates CD4+ T cell activation-induced cell death by metalloproteinase-dependent FasL shedding.  Toxicological Sciences, 92:103-14, 2006. 
  • Pumford, N.R., and Gilbert, K.M.  Autoimmunity Hepatitis.  Encyclopedic Reference of Immunotoxicology, Vohr, Hans-Wener (Ed), Springer Publishing Co., 2005.
  • Blossom, S.J., Pumford, N.R. and Gilbert, K.M. Activation and apoptosis of CD4+ T cells following in vivo exposure to two common environmental toxicants, trichloroacetaldehyde hydrate and trichloroacetic acid.  Journal of Autoimmunity, 23: 211-220, 2004
  • Gilbert, K.M., Whitlow, A., and Pumford, N.R. Environmental contaminant and disinfection by-product trichloroacetaldehyde stimulates T cells in vitro.  International Immunopharmacology 4:25-36, 2004.
  • Griffin, J.M., Gilbert, K.M., and Pumford, N.R.  CD4+ T cell activation and induction of autoimmune hepatitis following trichloroethylene treatment in MRL+/+ mice.  Toxicological Sciences 57:345-352, 2000.
  • Griffin, J.M., Gilbert, K.M., and Pumford, N.R.  Inhibition of CYP2E1 reverses CD4+ T cell alterations in trichloroethylene-treated MRL+/+ mice. Toxicological Sciences  54:384-389, 2000.
  • Griffin, J.M., Blossom, S.J., Jackson, S.K., Gilbert, K.M., and Pumford, N.R.  Trichloroethylene accelerates an autoimmune response in association with Th1 T cell activation in MRL+/+ mice.  Immunopharmacology  46:123-137,  2000.

Sarah Blossom, Ph.D., Associate Center Director, Assistant Professor of Pediatrics

Research Focus:Neuroimmune effects of developmental exposure to TCE

In children, the immune system is particularly sensitive to the effects of toxicant exposure, and consequences may not be detected until later in life.  ABI-funded research has led to the discovery that very that TCE promotes immune cell inflammation particularly early on following continuous maternal and early life exposure.  Low-level TCE exposed male mice also promoted adverse neurologic and behavioral deficits.  There is considerable cross-talk between the developing immunologic and neurologic systems during early development.  Current research will focus on the effects that exposure to traces of TCE during fetal, neonatal, and early life has on both neuroimmune functions.  This research has important implications on the development of neurologic and neurodevelopmental disorders, such as autism, Parkinson’s disease, and schizophrenia, which also involve immune dysfunction. 

Research Focus: Maternal cigarette smoke exposure and neuroimmune modulation
One of the goals of our center is to expand our research to include other environmental pollutants.  In collaboration with investigators at ASU, this research will study the impact of maternal smoking on the expression of nicotine-sensitive acetylcholine receptors (nAChR) in the developing brain and immune system.  Our hypothesis is that alterations in nAChR will mediate immune suppression and altered neural development in offspring of mothers who smoke during pregnancy.  This research promises to provide a potential breakthrough in understanding the health consequences of maternal smoking in children.

Click Here to View Dr. Blossom's Publications
  1. Gilbert, K.M., Nelson, A.R, Cooney, C.A., Reisfeld, B., and Blossom, S.J. Epigenetic alterations may regulate temporary reversal of CD4+ T cell activation caused by trichloroethylene exposure. Toxicol. Sci. 2012 May;127(1):169-78. Epub 2012 Mar 9.
  2. Blossom S.J., Melnyk, S., Cooney C.A., Gilbert K.M., and James, S.J. Postnatal exposure to trichloroethylene alters glutathione redox homeostasis, methylation potential, and neurotrophin expression in the mouse hippocampus. Neurotoxicology. Mar 7, 2012 [Epub ahead of print].
  3. Gilbert, KM, Rowley, B, Gomez-Acevedo, H, Blossom SJ. Co-exposure to mercury increases immunotoxicity of trichloroethylene. Toxicol. Sci. 2010. 119:281-292.
  4. James SJ, Rose S, Melnyk S, Jernigan S, Blossom S, Pavliv O, Gaylor DW. Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism. FASEB J. 2009 Aug; 23(8): 2371-83. Epub 2009 March 23.
  5. Gilbert KM, Przybyla B, Pumford NR, Han T, Fuscoe J, Schnackenberg LK, Holland RD, Doss JC, Macmillan-Crow LA, Blossom SJ. Delineating liver events in trichloroethylene-induced autoimmune hepatitis. Chem. Res. Toxicol. 2009. April 22 (4) 626-632.
  6. Gilbert KM, Blossom SJ, Pumford NR. Comments on "Lifetime exposure to trichloroethylene (TCE) does not accelerate autoimmune disease in MRL+/- mice. J. Env. Sci. Health Tox. Hazard Subst. Environ. Eng. 2009. Jan. 44 (1): 16; author reply 117-22.
  7. Blossom SJ, Doss JC, Hennings LJ, Jernigan S, Melnyk S, James SJ. Developmental exposure to trichloroethylene promotes CD4+ T cell differentiation and hyperactivity in association with oxidative stress and neurobehavioral deficits in MRL+/+ mice, Toxicology and Applied Pharmacology 2008 Sep 15;231(3):344-53. Epub 2008 May 20.344-353.
  8. Blossom SJ, Doss JC. Developmental exposure to the environmental toxicant trichloroethylene alters central and peripheral immune function in autoimmune-prone MRL+/+ mice. J Immunotox. 2007 Apr-Jun; 4(2): 129-41.
  9. Blossom SJ, Doss JC, Gilbert KM. Chronic exposure to a trichloroethylene metabolite in autoimmune-prone MRL+/+ mice promotes immune modulation and alopecia. Toxicol Sci. 2007 Feb; 95 (2): 401-11. Epub 2006 Oct 31.
  10. Gilbert KM, Pumford NR, Blossom SJ. Environmental Contaminant trichloroethylene promotes autoimmune disease and inhibits T-cell apoptosis in MRL+/+ mice. J Immunotox. 2006 Oct-Dec; 3 (4) 263-67.
  11. Blossom SJ, Doss JC, Gilbert KM. Ability of Environmental Toxicant trichloroethylene to promote immune pathology is strain specific. J Immunotox. 2006 Oct-Dec; 3 (4) 179-87.
  12. Blossom SJ, Gilbert KM. Exposure to an environmental toxicant, trichloroethylene, attenuates CD4+ T cell activation-induced cell death by metalloproteinase-dependent FasL shedding. Toxicol Sci. 2006 Jul; 92 (1) 103-14. Epub 2006 Apr 26.
  13. Blossom SJ, Pumford NR, Gilbert KM. Activation and attenuation of apoptosis of CD4+ T cells following in vivo exposure to two common environmental toxicants, trichloroacetaldehyde hydrate and trichloroacetic acid. J Autoimmun. 2004 Nov; 23 (3): 211-20.
  14. Griffin JM, Blossom, SJ, Jackson SK, Gilbert, KM, Pumford, NR. Trichloroethylene accelerates an autoimmune response by Th1 T cell activation in MRL+/+ mice. Immunopharmacology. 2000 Feb; 46 (2): 123-37.

Other ACEER Personnel

Brannon Broadfoot, B.S.
Laboratory Technician

Craig Cooney, Ph.D.
Epigenetics Consultant

Meagan Kreps, B.S.
Laboratory Technician

Rachel Lee, B.A.
Laboratory Technician

Jenny Rau, M.S.
Laboratory Technician

Presentations
  1. Gilbert, KM. Trichloroethylene-induced autoimmunity; dependence on metabolism and genetic susceptibility, In Workshop entitled “Autoimmunity versus systemic hypersensitivity: commonalities useful for toxicity testing, Society of Toxicology Annual Meeting, Washington, DC, 2011.

  2. Asghar SJ, Griebel ML, Blossom SJ, Williamson R, Maham SA, Gomez-Acevedo H, James SJ. Plasma Inflammatory and Oxidative Stress Markers in Autistic Children with Suspected Subclinical Seizures. Presented at the 40th meeting of the Child Neurology Society, Savannah, GA. Oct., 2011.

  3. Blossom SJ, Melnyk S, Gilbert KM, James SJ. Differential Expression of Neuroimmune Mediators Following Postnatal Exposure to Trichloroethylene. Presented at the 27th International Neurotoxicology Conference; Environmentally Triggered Neurodevelopmental Disorders: Focus on Endocrine Disruption and Sex Differences in Autism, ADHD, and Schizophrenia, Research Triangle Park, NC. October 30-November 2, 2011.

  4. Gilbert, KM. Chaired Poster Session: “Epigenetics” at the 51st Annual Society of Toxicology meeting, San Francisco, CA, March, 2012.

  5. Gilbert, KM, Nelson, A, Cooney, C, and Blossom, S. Subchronic trichloroethylene exposure alters epigenetic processes in CD4+ T cells. 51st Annual Society of Toxicology meeting, San Francisco, CA, March, 2012.

  6. Gilbert, KM. Chronic exposure to water pollutant trichloroethylene promotes autoimmune hepatitis and induces epigenetic alterations in CD4+ T cells; Special Symposia entitled “The role of environmental exposures in the development of autoimmune disease”, at 99th American Association of Immunologists meeting in Boston, MA, May 7, 2012.

 

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University of Arkansas for Medical Sciences

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University of Central Arkansas

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Kathleen Gilbert gilbertkathleenm@uams.edu

Sarah Blossom blossomsarah@uams.edu

 

 

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