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. 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
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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

Detail Information

Publications10

  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. 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...
  3. 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...
  4. 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...
  5. 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...
  6. 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...
  7. 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...
  8. 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
    ....
  9. 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...
  10. 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...