Sarah J Blossom

Summary

Affiliation: University of Arkansas for Medical Sciences
Country: USA

Publications

  1. ncbi request reprint Activation and attenuation of apoptosis of CD4+ T cells following in vivo exposure to two common environmental toxicants, trichloroacetaldehyde hydrate and trichloroacetic acid
    Sarah J Blossom
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, 1120 Marshall Street, Little Rock, AR 72205, USA
    J Autoimmun 23:211-20. 2004
  2. doi request reprint Trichloroethylene alters central and peripheral immune function in autoimmune-prone MRL(+/+) mice following continuous developmental and early life exposure
    Sarah J Blossom
    Department of Pediatrics, Arkansas Children s Hospital Research Institute, University of Arkansas for Medical Sciences College of Medicine, Little Rock, Arkansas 72202, USA
    J Immunotoxicol 4:129-41. 2007
  3. pmc Inflammatory and oxidative stress-related effects associated with neurotoxicity are maintained after exclusively prenatal trichloroethylene exposure
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, USA Electronic address
    Neurotoxicology . 2016
  4. pmc Metabolic changes and DNA hypomethylation in cerebellum are associated with behavioral alterations in mice exposed to trichloroethylene postnatally
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, USA
    Toxicol Appl Pharmacol 269:263-9. 2013
  5. doi request reprint Increased maternal cytokine production and congenital heart defects
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, USA
    J Reprod Immunol 97:204-10. 2013
  6. pmc Postnatal exposure to trichloroethylene alters glutathione redox homeostasis, methylation potential, and neurotrophin expression in the mouse hippocampus
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, USA
    Neurotoxicology 33:1518-27. 2012
  7. doi request reprint Developmental exposure to trichloroethylene promotes CD4+ T cell differentiation and hyperactivity in association with oxidative stress and neurobehavioral deficits in MRL+/+ mice
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 1120 Marshall Street, Little Rock, AR 72202, USA
    Toxicol Appl Pharmacol 231:344-53. 2008
  8. ncbi request reprint Chronic exposure to a trichloroethylene metabolite in autoimmune-prone MRL+/+ mice promotes immune modulation and alopecia
    Sarah J Blossom
    Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Toxicol Sci 95:401-11. 2007
  9. ncbi request reprint Exposure to a metabolite of the environmental toxicant, trichloroethylene, attenuates CD4+ T cell activation-induced cell death by metalloproteinase-dependent FasL shedding
    Sarah J Blossom
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Toxicol Sci 92:103-14. 2006
  10. doi request reprint Delineating liver events in trichloroethylene-induced autoimmune hepatitis
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Chem Res Toxicol 22:626-32. 2009

Detail Information

Publications17

  1. ncbi request reprint Activation and attenuation of apoptosis of CD4+ T cells following in vivo exposure to two common environmental toxicants, trichloroacetaldehyde hydrate and trichloroacetic acid
    Sarah J Blossom
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, 1120 Marshall Street, Little Rock, AR 72205, USA
    J Autoimmun 23:211-20. 2004
    ..By demonstrating that TCAH and TCA can activate CD4+ T cells and inhibit their apoptosis following in vivo exposure represents a mechanism by which environmental toxicants may induce or accelerate the development of autoimmune disease...
  2. doi request reprint Trichloroethylene alters central and peripheral immune function in autoimmune-prone MRL(+/+) mice following continuous developmental and early life exposure
    Sarah J Blossom
    Department of Pediatrics, Arkansas Children s Hospital Research Institute, University of Arkansas for Medical Sciences College of Medicine, Little Rock, Arkansas 72202, USA
    J Immunotoxicol 4:129-41. 2007
    ..Future studies will address the possibility that early-life exposure to TCE may alter some aspect of self tolerance in the thymus, leading to autoimmune disease later in life...
  3. pmc Inflammatory and oxidative stress-related effects associated with neurotoxicity are maintained after exclusively prenatal trichloroethylene exposure
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, USA Electronic address
    Neurotoxicology . 2016
    ..These results suggested that the prenatal period is a critical stage of life by which the developing CNS and immune system are susceptible to long-lasting changes mediated by TCE...
  4. pmc Metabolic changes and DNA hypomethylation in cerebellum are associated with behavioral alterations in mice exposed to trichloroethylene postnatally
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, USA
    Toxicol Appl Pharmacol 269:263-9. 2013
    ..The results show for the first time that postnatal exposure to TCE causes key metabolic changes in the cerebellum that may contribute to global DNA methylation deficits and behavioral alterations in TCE-exposed mice...
  5. doi request reprint Increased maternal cytokine production and congenital heart defects
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, USA
    J Reprod Immunol 97:204-10. 2013
    ..This information could pave the way toward maternal immunotherapeutic intervention to prevent CHDs, and novel biomarker discovery to improve pre-natal diagnosis...
  6. pmc Postnatal exposure to trichloroethylene alters glutathione redox homeostasis, methylation potential, and neurotrophin expression in the mouse hippocampus
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, USA
    Neurotoxicology 33:1518-27. 2012
    ..Our results demonstrate that low-level postnatal and early life TCE exposure modulates neurotrophin gene expression in the mouse hippocampus and may provide a mechanism for TCE-mediated neurotoxicity...
  7. doi request reprint Developmental exposure to trichloroethylene promotes CD4+ T cell differentiation and hyperactivity in association with oxidative stress and neurobehavioral deficits in MRL+/+ mice
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 1120 Marshall Street, Little Rock, AR 72202, USA
    Toxicol Appl Pharmacol 231:344-53. 2008
    ..The results demonstrated that developmental and early life TCE exposure modulated immune function and may have important implications for neurodevelopmental disorders...
  8. ncbi request reprint Chronic exposure to a trichloroethylene metabolite in autoimmune-prone MRL+/+ mice promotes immune modulation and alopecia
    Sarah J Blossom
    Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Toxicol Sci 95:401-11. 2007
    ..Taken together, a chronic exposure to TCAH promotes alopecia and skin inflammation. The early effects of TCAH on MMP-7 levels may provide a mechanism by which TCAH promotes skin pathology...
  9. ncbi request reprint Exposure to a metabolite of the environmental toxicant, trichloroethylene, attenuates CD4+ T cell activation-induced cell death by metalloproteinase-dependent FasL shedding
    Sarah J Blossom
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Toxicol Sci 92:103-14. 2006
    ..This represents a mechanism by which an environmental trigger inhibits AICD in CD4+ T cells and may thereby promote CD4+ T cell-mediated autoimmune disease...
  10. doi request reprint Delineating liver events in trichloroethylene-induced autoimmune hepatitis
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Chem Res Toxicol 22:626-32. 2009
    ....
  11. pmc Chronic exposure to water pollutant trichloroethylene increased epigenetic drift in CD4(+) T cells
    Kathleen M Gilbert
    Departments of Microbiology and Immunology, and Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, AR 72202, USA
    Epigenomics 8:633-49. 2016
    ..We examined here whether TCE altered gene-specific DNA methylation in CD4(+) T cells as a possible mechanism of immunotoxicity...
  12. pmc Epigenetic alterations may regulate temporary reversal of CD4(+) T cell activation caused by trichloroethylene exposure
    Kathleen M Gilbert
    Arkansas Children s Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72202, USA
    Toxicol Sci 127:169-78. 2012
    ..Thus, these results described the biphasic nature of TCE-induced alterations in CD4(+) T cell function and suggested that these changes represented potentially reversible alterations in epigenetic processes...
  13. pmc Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells
    Kathleen M Gilbert
    University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, AR 72202, United States Electronic address
    Toxicol Lett 260:1-7. 2016
    ..Taken together, the CpG sites of the Ifng promoter in effector/memory CD4+ T cells were especially sensitive to the effects of TCE exposure, which may help explain the regulatory effect of the chemical on this gene...
  14. pmc Coexposure to mercury increases immunotoxicity of trichloroethylene
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, College of Medicine, Arkansas, USA
    Toxicol Sci 119:281-92. 2011
    ..Coexposure to TCE and HgCl(2) also generated a unique liver-specific antibody response not found in mice exposed to a single toxicant. This finding stresses the importance of including mixtures in assessments of chemical immunotoxicity...
  15. doi request reprint Environmental contaminant trichloroethylene promotes autoimmune disease and inhibits T-cell apoptosis in MRL(+/+) mice
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    J Immunotoxicol 3:263-7. 2006
    ....
  16. doi request reprint Ability of trichloroethylene metabolite to promote immune pathology is strain-specific
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    J Immunotoxicol 3:179-87. 2006
    ..Taken together, it appears that the ability of TCAH to promote immune-mediated pathology is strain-specific and may require an autoimmune-prone genetic background...
  17. pmc Modeling toxicodynamic effects of trichloroethylene on liver in mouse model of autoimmune hepatitis
    Kathleen M Gilbert
    University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, AR 72202, USA Electronic address
    Toxicol Appl Pharmacol 279:284-93. 2014
    ..This information was used to create a novel toxicodynamic model of IL-6-mediated TCE-induced liver inflammation. ..