Erin Steinbach
· Assistant Professor of MedicineUniversity of North Carolina at Chapel Hill · Toxicology
Active 1989–2026
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About
Erin Steinbach, MD, PhD, is an Assistant Professor of Medicine at the University of North Carolina at Chapel Hill, affiliated with the Curriculum in Toxicology & Environmental Medicine. Her clinical interests primarily focus on food allergy, peanut allergy, allergen immunotherapy, and eosinophilic disorders. Her core research areas include peanut allergy, food allergy, eosinophilic gastrointestinal disease (EGID), and gastrointestinal dysfunction in food allergy. Dr. Steinbach's expertise extends to various clinical conditions such as allergic rhinitis, asthma, atopic dermatitis, stinging insect allergy, drug allergy, drug desensitization, eosinophilic disorders, chronic idiopathic urticaria and angioedema, hereditary and acquired angioedema, mast cell disorders, and primary and secondary immunodeficiency. She completed her undergraduate studies at Gustavus Adolphus College, earned her medical degree and PhD from the University of North Carolina at Chapel Hill, and completed her residency, fellowship, and further training at UNC Hospitals. Her work integrates clinical practice with research focused on food allergy and gastrointestinal inflammation.
Research topics
- Biology
- Internal medicine
- Medicine
- Cell biology
- Gastroenterology
- Immunology
- Pathology
- Cancer research
Selected publications
Frontiers in Immunology · 2021 · 31 citations
. Overall, these results demonstrate several factors associated with enteral sensitization in CC027/GeniUnc mice, including diminished total fecal IgA, increased allergen absorption and altered gut microbiome composition. Furthermore, peanuts and tree nuts may have inherent properties distinct from milk and eggs that contribute to allergy.
Increased colonic expression of ACE2 associates with poor prognosis in Crohn’s disease
Scientific Reports · 2021 · 24 citations
The host receptor for SARS-CoV-2, angiotensin-converting enzyme 2 (ACE2), is highly expressed in small intestine. Our aim was to study colonic ACE2 expression in Crohn's disease (CD) and non-inflammatory bowel disease (non-IBD) controls. We hypothesized that the colonic expression levels of ACE2 impacts CD course. We examined the expression of colonic ACE2 in 67 adult CD and 14 NIBD control patients using RNA-seq and quantitative (q) RT-PCR. We validated ACE2 protein expression and localization…
Cellular and Molecular Gastroenterology and Hepatology · 2020 · 22 citations
BACKGROUND & AIMS: Intestinal epithelial cell (IEC) barrier dysfunction is critical to the development of Crohn's disease (CD). However, the mechanism is understudied. We recently reported increased microRNA-31-5p (miR-31-5p) expression in colonic IECs of CD patients, but downstream targets and functional consequences are unknown. METHODS: microRNA-31-5p target genes were identified by integrative analysis of RNA- and small RNA-sequencing data from colonic mucosa and confirmed by quantitative po…
BET Protein Inhibition Regulates Macrophage Chromatin Accessibility and Microbiota-Dependent Colitis
Frontiers in Immunology · 2022-03-24 · 10 citations
articleOpen accessIntroduction In colitis, macrophage functionality is altered compared to normal homeostatic conditions. Loss of IL-10 signaling results in an inappropriate chronic inflammatory response to bacterial stimulation. It remains unknown if inhibition of bromodomain and extra-terminal domain (BET) proteins alters usage of DNA regulatory elements responsible for driving inflammatory gene expression. We determined if the BET inhibitor, (+)-JQ1, could suppress inflammatory activation of macrophages in Il1…
UNC Libraries · 2020-11-05 · 7 citations
articleOpen accessSenior authorThere are many different animal models available for studying the pathogenesis of human inflammatory bowel diseases (IBD), each with its own advantages and disadvantages. We describe here an experimental colitis model that is initiated by adoptive transfer of syngeneic splenic CD4+CD45RBhigh T cells into T and B cell deficient recipient mice. The CD4+CD45RBhigh T cell population that largely consists of naïve effector cells is capable of inducing chronic intestinal inflammation, closely resembli…
Recent grants
NIH · $157k · 2015
Frequent coauthors
- 21 shared
Scott E. Plevy
Protagonist Therapeutics (United States)
- 21 shared
Shehzad Z. Sheikh
University of North Carolina at Chapel Hill
- 15 shared
Terrence S. Furey
University of North Carolina at Chapel Hill
- 11 shared
Matthew R. Schaner
University of North Carolina at Chapel Hill
- 11 shared
Taku Kobayashi
Kitasato Institute Hospital
- 10 shared
Jonathan J. Hansen
University of Nevada, Las Vegas
- 10 shared
Takahiko Toyonaga
Jikei University School of Medicine
- 10 shared
Hans Herfarth
University of North Carolina at Chapel Hill
Labs
Education
- 2006
Ph.D., Toxicology
University of North Carolina at Chapel Hill
- 2002
M.S., Toxicology
University of North Carolina at Chapel Hill
- 2000
B.S., Toxicology
University of North Carolina at Chapel Hill
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