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 (H 2 S)-producing bacteria, particularly Desulfovibrio species, in disrupting cutaneous lipid homeostasis and contributing to SD in IBD patients. Elevated H 2 S 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, H 2 S biochemistry, and skin barrier research. Advanced techniques such as 16S rRNA sequencing, lipidomics, and H 2 S quantification were analyzed to elucidate the connections between gut-derived H 2 S and skin inflammation. Inclusion criteria focused on studies involving IBD patients with concurrent SD or elevated H 2 S-producing bacterial populations. Results : IBD-associated gut dysbiosis is characterized by increased Desulfovibrio species and elevated H 2 S levels, which impair epithelial integrity and contribute to systemic inflammation. H 2 S 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 H 2 S concentration thresholds and specific pathways linking gut and skin inflammation. Conclusions : Targeting H 2 S-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.
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Lipid Metabolism
Cutaneous Inflammation
Microbiome Therapy
Pro-Inflammatory Cytokines
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