Gut Dysbiosis in Inflammatory Skin Diseases: Lessons From Atopic Dermatitis, Psoriasis, and Rosacea With Potential Implications for Hidradenitis Suppurativa

Background Hidradenitis suppurativa (HS) is a chronic inflammatory skin disorder characterized by recurrent nodules, abscesses, and sinus tract formation. Emerging studies suggest that dysbiosis of both the gut and cutaneous microbiome may contribute to the pathogenesis of HS. The modulation of the gut–skin axis using probiotic supplements is gaining interest as a potential adjunctive therapy in inflammatory dermatoses. Objective To review the current evidence on microbiome alterations in HS and to evaluate the theoretical and clinical rationale for probiotic interventions. Methods We conducted a structured narrative review of the published literature examining HS‐associated microbiome dysbiosis, mechanistic pathways of the gut–skin axis, and the therapeutic rationale for probiotics in HS and related inflammatory dermatoses. Literature searches were performed in PubMed/MEDLINE and Scopus up to December 2025 using combinations of the following keywords and Medical Subject Heading (MeSH) terms: “hidradenitis suppurativa,” “acne inversa,” “microbiome,” “gut microbiota,” “skin microbiota,” “gut–skin axis,” “dysbiosis,” “probiotics,” “prebiotics,” “synbiotics,” “diet,” and “inflammatory skin disease.” Original articles, systematic reviews, meta‐analyses, mechanistic studies, and relevant clinical studies published in English were considered. Articles unrelated to HS, microbiome modulation, or inflammatory skin disease were excluded. Reference lists of included studies were additionally screened to identify further relevant publications. Results HS has been associated with alterations in both the skin and the gut microbiota, including an enrichment of anaerobic species and a reduced microbial diversity. Dysregulated immune pathways, altered tryptophan metabolism, and impaired barrier function may contribute to disease perpetuation. While direct randomized controlled trials that evaluate probiotics in HS are lacking, evidence from psoriasis, eczema, and rosacea suggests immunomodulatory and anti‐inflammatory benefits of specific probiotic strains. Mechanistic studies suggest that probiotic supplementation may influence the pathophysiology of HS by modulating regulatory T‐cell responses, suppressing proinflammatory cytokines, restoring epithelial barrier integrity, and producing beneficial microbial metabolites. Conclusion Although microbiome dysbiosis appears increasingly relevant to HS pathophysiology, current evidence remains insufficient to support specific probiotic interventions in clinical practice. Existing probiotic data are largely extrapolated from other inflammatory skin diseases and therefore warrant further investigation. Robust randomized controlled trials about HS are required before clinical recommendations can be made to determine the efficacy, optimal strains, and long‐term safety in HS patients.