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

• Paneth Cell-Derived Lysozyme Is Deficient In Peanut Allergy

  Journal of Allergy and Clinical Immunology · 2026-02-01

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Myeloid Cell Adhesion Molecule 1 (CADM1) Promotes Proinflammatory Signaling in Human Inflammatory Bowel Diseases

  Cellular and Molecular Gastroenterology and Hepatology · 2025-08-27 · 3 citations

  articleOpen access

  BACKGROUND & AIMS: Cytotoxic T cells have been postulated to facilitate the destruction of intestinal epithelium in inflammatory bowel diseases (IBDs). CADM1, which encodes a membrane adhesion protein that can bind the T cell receptor CRTAM, was markedly up regulated in colons of IBD patients compared with non-IBD (NIBD) patients. METHODS: We performed comprehensive small RNA and RNA profiling on colon tissue from IBD and NIBD control patients in addition to characterizing the serum cleaved ectodomain of CADM1 (sCADM1) function in lamina propria mononuclear cells isolated from these patients. Last, a conditional loss-of-function mouse was developed to assess Cadm1 function in the myeloid compartment during chemical-induced colitis. RESULTS: T cells within colons of ulcerative colitis patients compared with NIBD patients. Conditional deletion of Cadm1 in myeloid cells resulted in reduced numbers of activated T cell populations and protected mice from chemical-induced colitis. Similarly, administration of a Cadm1 "neutralizing" antibody, which binds its extracellular domain reduced tissue inflammation and breakdown of the intestinal epithelium and crypts after induction of colitis in mice. Last, serum levels of sCADM1 were elevated in IBD patients compared with NIBD control subjects and treatment of lamina propria mononuclear cells with recombinant sCADM1 enhanced inflammatory STAT3 phosphorylation. CONCLUSIONS: CADM1 is a mediator of proinflammatory signaling cascades in the colon and a potential therapeutic target for the IBDs.

  PublisherDOI

• Fecal IgA, Antigen Absorption, and Gut Microbiome Composition Are Associated With Food Antigen Sensitization in Genetically Susceptible Mice

  UNC Libraries · 2025-01-16

  articleOpen access1st authorCorresponding

  Food allergy is a potentially fatal disease affecting 8% of children and has become increasingly common in the past two decades. Despite the prevalence and severe nature of the disease, the mechanisms underlying sensitization remain to be further elucidated. The Collaborative Cross is a genetically diverse panel of inbred mice that were specifically developed to study the influence of genetics on complex diseases. Using this panel of mouse strains, we previously demonstrated CC027/GeniUnc mice, but not C3H/HeJ mice, develop peanut allergy after oral exposure to peanut in the absence of a Th2-skewing adjuvant. Here, we investigated factors associated with sensitization in CC027/GeniUnc mice following oral exposure to peanut, walnut, milk, or egg. CC027/GeniUnc mice mounted antigen-specific IgE responses to peanut, walnut and egg, but not milk, while C3H/HeJ mice were not sensitized to any antigen. Na&iuml;ve CC027/GeniUnc mice had markedly lower total fecal IgA compared to C3H/HeJ, which was accompanied by stark differences in gut microbiome composition. Sensitized CC027/GeniUnc mice had significantly fewer CD3⁺ T cells but higher numbers of CXCR5⁺ B cells and T follicular helper cells in the mesenteric lymph nodes compared to C3H/HeJ mice, which is consistent with their relative immunoglobulin production. After oral challenge to the corresponding food, peanut- and walnut-sensitized CC027/GeniUnc mice experienced anaphylaxis, whereas mice exposed to milk and egg did not. Ara h 2 was detected in serum collected post-challenge from peanut-sensitized mice, indicating increased absorption of this allergen, while Bos d 5 and Gal d 2 were not detected in mice exposed to milk and egg, respectively. Machine learning on the change in gut microbiome composition as a result of food protein exposure identified a unique signature in CC027/GeniUnc mice that experienced anaphylaxis, including the depletion of <em>Akkermansia</em>. 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.

  PublisherDOI

• Intestinal epithelial cell barrier dysfunction and elevated Angiopoietin-like 4 identified in orally susceptible peanut allergy model

  UNC Libraries · 2024-08-14

  articleOpen access

  To the editors: Peanut remains the number one cause of death due to food-related anaphylaxis. Co-factors (e.g., febrile illness, vigorous exercise) that modify the severity of food allergic reaction are known to increase intestinal epithelial cell (IEC) barrier permeability, and patients with peanut allergy have higher serum levels of a major peanut allergen (Ara h 6) after peanut ingestion. Yet, we do not understand basic interactions between peanut and IECs.

  PublisherDOI

• Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Epithelial Barrier Integrity in Patients With Crohn's Disease

  UNC Libraries · 2024-08-14

  articleOpen access
  PublisherDOI

• Compositional and functional modifications of the Jejunal microbiota in human obesity Emilie Steinbach, Eugeni Belda, Rohia Alili, Véronique Pelloux, Davide Masi, Solia Adriouch, Tiphaine Le Roy, Karine Clément

  Clinical Nutrition ESPEN · 2023-12-01

  article1st authorCorresponding
  PublisherDOI

• Su1557: DISCOVERY OF UNANNOTATED LNCRNAS IN COLONIC TISSUE OF CD PATIENTS WITH POTENTIAL ASSOCIATION TO DISEASE PHENOTYPES

  Gastroenterology · 2022-05-01

  article
  PublisherDOI

• Intestinal Barrier Dysfunction Accompanies Peanut Allergy In A Genetically-Susceptible Mouse Model And Identifies Angiopoietin-like 4 As A Biomarker

  Journal of Allergy and Clinical Immunology · 2022-02-01

  article1st authorCorresponding
  PublisherDOI

• BET Protein Inhibition Regulates Macrophage Chromatin Accessibility and Microbiota-Dependent Colitis

  UNC Libraries · 2022-03-29 · 1 citations

  articleOpen access1st authorCorresponding

  Introduction 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 Il10-/- mice. Methods We performed ATAC-seq and RNA-seq on Il10-/- bone marrow-derived macrophages (BMDMs) cultured in the presence and absence of lipopolysaccharide (LPS) with and without treatment with (+)-JQ1 and evaluated changes in chromatin accessibility and gene expression. Germ-free Il10-/- mice were treated with (+)-JQ1, colonized with fecal slurries and underwent histological and molecular evaluation 14-days post colonization. Results Treatment with (+)-JQ1 suppressed LPS-induced changes in chromatin at distal regulatory elements associated with inflammatory genes, particularly in regions that contain motifs for AP-1 and IRF transcription factors. This resulted in attenuation of inflammatory gene expression. Treatment with (+)-JQ1 in vivo resulted in a mild reduction in colitis severity as compared with vehicle-treated mice. Conclusion We identified the mechanism of action associated with a new class of compounds that may mitigate aberrant macrophage responses to bacteria in colitis.

  PublisherDOI

• Intestinal epithelial cell barrier dysfunction and elevated Angiopoietin‐like 4 identified in orally susceptible peanut allergy model

  Clinical & Experimental Allergy · 2022-11-06 · 2 citations

  letterOpen access1st author
  PublisherOA PDFDOI

Recent grants

• NIH Grant F30DK089692

  NIH · $157k · 2015

Frequent coauthors

• Scott E. Plevy

  Protagonist Therapeutics (United States)

  21 shared

• Shehzad Z. Sheikh

  University of North Carolina at Chapel Hill

  21 shared

• Terrence S. Furey

  University of North Carolina at Chapel Hill

  15 shared

• Matthew R. Schaner

  University of North Carolina at Chapel Hill

  11 shared

• Taku Kobayashi

  Kitasato Institute Hospital

  11 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

  10 shared

Labs

• Curriculum in Toxicology & Environmental MedicinePI

Education

• Ph.D., Toxicology

  University of North Carolina at Chapel Hill

  2006

• M.S., Toxicology

  University of North Carolina at Chapel Hill

  2002

• B.S., Toxicology

  University of North Carolina at Chapel Hill

  2000