The Role of the gut microbiome in psoriasis pathogenesis:evidence from human studies

نویسندگان

1 Skin Research Center,Shahid Beheshti University of medical sciences

2 Skin Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran

3 Musculoskeletal Injuries Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran

doi
10.22034/ijd.2025.540625.2080
چکیده

Background: Psoriasis is a chronic, immune-mediated skin disorder influenced by genetic predisposition, environmental triggers, and immune dysregulation. Emerging evidence suggests that alterations in the gut and skin microbiomes may contribute to disease pathogenesis and severity, highlighting the importance of the gut–skin axis. This systematic review aimed to synthesize current evidence on the association between microbiome alterations and psoriasis, focusing on compositional and functional changes in gut and skin microbial communities. Methods: A comprehensive literature search was conducted in MEDLINE, Embase, Web of Science, and Scopus for studies published up to December 2024. Observational studies employing culture-independent sequencing methods (e.g., 16S rRNA gene sequencing, metagenomics) that reported microbiome differences between psoriasis patients and healthy controls were included. Two reviewers independently screened the studies, extracted data, and assessed methodological quality.Results: Twenty-five studies, with sample sizes ranging from 13 to 300 participants, were included. Gut microbiome analyses revealed heterogeneous α-diversity findings but consistently demonstrated distinct β-diversity between psoriasis patients and controls. Dysbiosis patterns included a decreased abundance of beneficial commensals such as Faecalibacterium prausnitzii and Roseburia, alongside an enrichment of pro-inflammatory taxa, including Ruminococcus gnavus and Escherichia coli. Functional analyses linked these microbial alterations to impaired gut barrier integrity and systemic inflammation. Skin microbiome studies indicated increased levels of Staphylococcus and Streptococcus species, accompanied by decreased protective commensals, suggesting that localized dysbiosis amplifies cutaneous inflammation. Evidence also indicates that systemic therapies, such as IL-17A inhibitors, can partially restore microbial balance, underscoring the interplay between immune modulation and microbiome composition.Conclusion: Current evidence supports a strong association between alterations in the gut and skin microbiomes and psoriasis pathogenesis. Dysbiosis may contribute to immune dysregulation, barrier dysfunction, and systemic inflammation. Future large-scale, longitudinal, and multiomics studies are needed to clarify causal mechanisms and to explore microbiome-based diagnostic and therapeutic strategies for managing psoriasis.