TITLE:
Hydrogen Sulfide-Producing Gut Bacteria as a Trigger for Seborrheic Dermatitis in Ulcerative Colitis
AUTHORS:
Andrew Pugliese, David Matatov, Julia Vinagolu-Baur, Milana Stein, Alejandra Sataray-Rodriguez, Radhika Misra, Muhammad Hassan, Emily Deehan, Ryan Porter, Camile Delva
KEYWORDS:
Gut-Skin Axis, Seborrheic Dermatitis, Inflammatory Bowel Disease, Hydrogen Sulfide, Desulfovibrio, Dysbiosis, Lipid Metabolism, Cutaneous Inflammation, Microbiome Therapy, Pro-Inflammatory Cytokines
JOURNAL NAME:
Open Journal of Gastroenterology,
Vol.15 No.7,
July
7,
2025
ABSTRACT: Background and Objectives: The gut-skin axis is a critical pathway linking gut microbiota composition and skin health. Evidence suggests that dysbiosis in inflammatory bowel disease (IBD) may exacerbate seborrheic dermatitis (SD), a chronic inflammatory skin condition. This review investigates the role of hydrogen sulfide (H2S)-producing bacteria, particularly Desulfovibrio species, in disrupting cutaneous lipid homeostasis and contributing to SD in IBD patients. Elevated H2S production by these bacteria is hypothesized to drive systemic inflammation and cutaneous lipid dysregulation, providing new insights into the pathophysiology of SD in IBD populations. Methods: A comprehensive literature review was conducted, synthesizing findings from microbiome studies, H2S biochemistry, and skin barrier research. Advanced techniques such as 16S rRNA sequencing, lipidomics, and H2S quantification were analyzed to elucidate the connections between gut-derived H2S and skin inflammation. Inclusion criteria focused on studies involving IBD patients with concurrent SD or elevated H2S-producing bacterial populations. Results: IBD-associated gut dysbiosis is characterized by increased Desulfovibrio species and elevated H2S levels, which impair epithelial integrity and contribute to systemic inflammation. H2S dysregulation disrupts lipid metabolism in sebum, weakening the skin barrier and promoting overgrowth of Malassezia species, a key factor in SD pathogenesis. Pro-inflammatory cytokines, such as TNF-α and IL-17, are upregulated, exacerbating skin inflammation. Despite these insights, critical knowledge gaps remain regarding H2S concentration thresholds and specific pathways linking gut and skin inflammation. Conclusions: Targeting H2S-producing bacteria and gut dysbiosis holds promise for managing SD in IBD patients. Integrated therapeutic strategies, such as probiotics, prebiotics, and dietary modifications, may address the dual burden of gut and skin inflammation. Longitudinal studies and standardized methodologies are needed to advance understanding and improve outcomes in this population.