
Probiotics in Hidradenitis Suppurativa: Biologic Rationale vs. Clinical Evidence
Key Takeaways
- Cutaneous dysbiosis in HS features increased Porphyromonas, Prevotella, Peptoniphilus, and Fusobacterium with reduced Cutibacterium acnes and Staphylococcus epidermidis, potentially reinforced by tunnel biofilms and antibiotic tolerance.
- Limited gut studies report decreased microbial diversity and perturbed tryptophan metabolism with impaired aryl hydrocarbon receptor pathway activation, but causality versus inflammation-driven secondary change is unresolved.
HS microbiome studies fuel probiotic hype, but a new review finds evidence too thin for routine use and highlights key research gaps.
Growing evidence suggests that alterations in both the skin and gut microbiome may contribute to the development and persistence of hidradenitis suppurativa (HS), prompting interest in microbiome-targeted therapies such as probiotics.1 However, a new narrative review concludes that despite biologic plausibility and encouraging findings from other inflammatory skin diseases, there is currently insufficient evidence to recommend probiotic supplementation as part of routine HS management.2
The review examined published literature through December 2025 on HS-associated microbiome dysbiosis, the gut–skin axis, and probiotic interventions. Because randomized controlled trials evaluating probiotics specifically in HS are lacking, the authors also evaluated mechanistic and clinical evidence from psoriasis, atopic dermatitis, rosacea, and inflammatory bowel disease to assess whether those findings may have implications for HS.
Microbial Dysbiosis in HS
Recent microbiome studies suggest that both the skin and gut microbial communities are altered in HS. On the skin, investigators consistently observed a shift away from healthy commensal organisms toward polymicrobial anaerobic bacteria, including Porphyromonas, Prevotella, Peptoniphilus, and Fusobacterium. At the same time, beneficial organisms such as Cutibacterium acnes and Staphylococcus epidermidis appear to be depleted. Biofilm formation within HS tunnels may further contribute to chronic inflammation, recurrent disease, and reduced antibiotic effectiveness.
Beyond the skin, several small studies have reported reduced gut microbial diversity and changes in bacterial composition among patients with HS. Investigators also identified abnormalities in tryptophan metabolism and impaired activation of the aryl hydrocarbon receptor pathway, findings that may influence immune regulation and barrier function. However, the authors caution that these studies remain small and observational, making it impossible to determine whether gut dysbiosis is a cause of HS or simply a consequence of chronic inflammation.
The Gut–Skin Axis & Potential Mechanisms
The review highlights the gut–skin axis as a potential framework linking intestinal microbes with cutaneous inflammation. Microbial metabolites, particularly short-chain fatty acids such as butyrate, acetate, and propionate, may help regulate immune responses by promoting regulatory T cells while suppressing proinflammatory cytokines. Altered intestinal barrier function and increased systemic exposure to bacterial products have also been proposed as contributors to inflammatory skin disease, although direct evidence in HS remains limited.
Given the absence of HS-specific intervention studies, much of the current rationale for probiotics comes from research in other inflammatory dermatoses.
- In atopic dermatitis, multistrain probiotic formulations containing Lactobacillus and Bifidobacterium species have demonstrated modest improvements in disease severity in systematic reviews.
- In psoriasis, probiotic supplementation has been associated with reductions in inflammatory markers and modest clinical improvement, although studies vary considerably in probiotic strains, treatment duration, and outcome measures.
- In rosacea, patients have shown clinical improvement when probiotics were combined with standard therapy.
Across these conditions, proposed mechanisms include modulation of regulatory T-cell responses, suppression of inflammatory cytokines such as tumor necrosis factor-α, IL-1β, IL-6, and IL-17, enhancement of epithelial barrier integrity, production of beneficial microbial metabolites, and competitive inhibition of pathogenic bacteria. Nevertheless, the authors stress that these findings cannot be directly extrapolated to HS because of important differences in disease biology and microbiology.
Dietary Considerations & Barriers to Clinical Use
The review also discusses dietary approaches that may influence the gut microbiome. Western dietary patterns have been associated with inflammatory pathways relevant to HS, whereas Mediterranean-style eating patterns and fiber-rich diets may promote production of beneficial microbial metabolites. Although these strategies appear promising, the evidence remains limited and does not establish a direct therapeutic benefit in HS.
The authors identify several major barriers to clinical implementation of probiotics, including;
- Lack of randomized controlled trials
- Inconsistent microbiome study methods
- Variability in probiotic formulations
- Uncertainty regarding optimal strains, dosing, treatment duration, and long-term safety
- Individual variation driven by host genetics, existing microbiome composition, and environmental factors
Until higher-quality evidence becomes available, the review recommends that clinicians continue to rely on established evidence-based HS therapies. While probiotics remain biologically plausible as adjunctive treatments, they should currently be considered investigational rather than incorporated into routine clinical care. Future randomized controlled trials will be needed to determine whether microbiome modulation can meaningfully improve outcomes for patients with HS and to identify which patients, if any, are most likely to benefit.
References
1. Zhao Y, Yu C, Zhang J, Yao Q, Zhu X, Zhou X. The gut‑skin axis: Emerging insights in understanding and treating skin diseases through gut microbiome modulation (Review). Int J Mol Med. 2025;56(6):210. doi:10.3892/ijmm.2025.5651
2. Semaani JMA, Abbas O, Kurban M, Gut Dysbiosis in Inflammatory Skin Diseases: Lessons From Atopic Dermatitis, Psoriasis, and Rosacea With Potential Implications for Hidradenitis Suppurativa. Dermatologic Therapy, 2026, 5815717, 9 pages, 2026. doi:10.1155/dth/5815717








