Sarah Blossom, PhD
Assistant Professor of Pediatrics, University of Arkansas for Medical Sciences
Phone: (501) 364-2861

Dr. Blossom's expertise and interests concern the areas of developmental immunotoxicology and reproductive immunology as described below:

Maternal Immune Modulation and Birth Defects

Maternal Immune Function and Congenital Heart Defects (Collaboration with Dr. Charlotte Hobbs)

Dr. Sarah Blossom, working with the Center for Birth Defects Research and Prevention group at ACHRI, conducted a preliminary study demonstrating cytokine alterations in plasma of women with a congenital heart defect-affected pregnancy. These data suggest that maternal immune dysfunction may play a role in the development of congenital heart defects. Dr. Blossom was awarded a CUMG grant entitled Establishing a link between maternal immune dysfunction and congenital heart defects (December 2007-December 2009) to further study immune function in women in mid trimester diagnosed with fetal congenital heart defect.  Recently, Drs. Blossom and Hobbs submitted a letter of intent to the CDC-National Birth Defects Prevention Study to evaluate polymorphisms in immune responses genes in congenital heart defects.  Dr. Blossom is also currently a co-investigator on the National Birth Defects Prevention Study (Hobbs PI).  Dr. Blossom recently submitted a grant to the American Heart Association and to the NIH (R03; 2/16/09) to study maternal immune modulation in a mouse model of congenital heart defects. 

Developmental Immunotoxicology and Neruo-Immunotoxicology

1.         Trichloroethylene

Dr. Blossom also conducts research with Dr. Kathleen Gilbert, who was recently awarded funding from a lawsuit settlement to conduct research into the toxicity of the common water pollutant trichloroethylene.  While Dr. Gilbert is concerned with adult trichloroethylene exposure, Dr. Blossom is primarily interested in developmental trichloroethylene exposure (exposure during pregnancy and early life) and has developed independent research in this area.

Children are particularly vulnerable to exposure to environmental chemicals. It has been found that approximately 10% of children 6-10 years of age have detectable levels of trichloroethylene, a common environmental chemical, in the blood. To determine the impact of perinatal trichloroethylene exposure, Dr. Sarah Blossom exposed mice throughout development (pregnancy and early life) to low levels of trichloroethylene. The offspring exhibited altered immune function. Remarkably, the young mice also showed abnormal social behavior and increased biomarkers of oxidative stress in the brain and developing immune system. These studies could potentially pave the way for a novel mouse model of autism and will be expanded through collaboration with Dr. Jill James’ laboratory. 

2.         Prenatal Cigarette Smoke Exposure

In collaboration with Dr. Dolan and Dr. Buchanan of Arkansas State University, received $60K for the Arkansas Biosciences Institute to study maternal smoking and neuroimmune modulation involving altered expression of nicotine sensitive acetylcholine receptors in the developing brain and immune system. The three researchers will use a mouse model of maternal cigarette smoke exposure to study the hypothesis that alterations in nicotine-sensitive acetylcholine receptors (nAChR) in the developing brain and immune system is a mechanism for the immune suppression and altered neural development observed 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.

Key Publications

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. Toxicol Appl Pharmacol. 2008 Sep 15;231(3):344-53.

Blossom SJ, Doss JC 2007. Trichloroethylene alters central and peripheral immune function in autoimmune-prone MRL+/+ mice following continuous developmental and early life exposure. Journal of Immunotoxicology 4(2) 129-141.

Blossom SJ, Gilbert KM 2006. 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(1) 103-114.

Blossom SJ, Pumford NR, Gilbert KM 2004. Activation and attenuation of apoptosis of CD4 + T cells following in vivo exposure to two common environmental toxicants, trichloroacetaldehyde hydrate and trichloroacetic acid. Journal of Autoimmunity 23(3) 211-20.

To find publications by Sarah Blossom, please visit Pubmed Central, a National Institutes of Health-operated site for electronic distribution of life sciences research reports.

Children's University Medical Group (CUMG) : The fetal basis of toxicant-induced autoimmunity

Arkansas Biosciences Institute