Presenter

Hailey Soares

Document Type

Poster

Publication Date

2026

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by impaired epidermal barrier function and immune dysregulation. Emerging evidence suggests that the gut microbiome plays a key role in immune signaling pathways involved in AD development and severity, particularly during early life. This project examined how the gut microbiome influences skin inflammation to determine key immunological mechanisms mediating AD symptomology and possible therapeutic strategies. Reduced microbial diversity and decreased abundance of short-chain fatty acid (SCFA)‚ producing anaerobes are consistently associated with increased AD risk. Dysbiosis disrupts immune tolerance by impairing regulatory T cell (Treg) function and promoting Th2 and Th17 mediated cytokine responses, including IL-4, IL-13, IL-6, and IL-17. These cytokines weaken epidermal barrier integrity, enhance IgE-mediated inflammation, and¬†increase skin sensitivity. Additionally, early-life factors such as antibiotic exposure, diet, and microbial colonization further influence immune maturation and AD susceptibility. The gut-skin axis provides a mechanistic framework linking intestinal microbial imbalance to systemic inflammation and cutaneous immune dysregulation. Improved understanding of gut microbiome-immune interactions offer promising avenues for novel preventive and therapeutic strategies, including dietary modulation, probiotics, and personalized microbiome-based interventions for atopic dermatitis.

Faculty Mentor

Nicole Urban, Ph.D.

Academic Discipline

College of Arts & Sciences

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