REVIEW article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders: Autoinflammatory Disorders
Psoriasis: Microbiome Dysbiosis and Pathogenic Mechanisms
Binghao Wang 1
Yi Zhang 1
Li Lin 1
Songyan Wang 1
Suqing Yang 2
1. Heilongjiang University of Chinese Medicine, Harbin, China
2. First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin, China
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Abstract
Abstract Psoriasis is a chronic immune-mediated inflammatory disease whose pathogenesis is a triad of genetic predisposition, immune dysregulation, and environmental triggers. This review provides a novel, in-depth synthesis arguing that microbial dysbiosis is not merely an associative phenomenon but a central regulatory node within this triad, actively shaping immune responses and clinical phenotypes. We move beyond cataloging microbial shifts to construct a detailed mechanistic framework of the gut-skin axis. Gut dysbiosis; characterized by reduced diversity, a diminished Bacteroidetes/Firmicutes ratio, and depleted SCFA producers, compromises intestinal barrier integrity, reduces systemic immunoregulatory tone via diminished SCFA signaling, and promotes Th17 polarization. This systemic inflammation is directly communicated to the skin. Concurrently, cutaneous dysbiosis, featuring Staphylococcus aureus dominance and fungal alterations, disrupts the local barrier, provides chronic antigenic stimulation, and amplifies IL-17-driven inflammation, creating a self-sustaining loop. Crucially, we analyze how specific infections (HCV, H. pylori, Streptococcus) act as environmental triggers by sharing or activating these very pathways. The bidirectional relationship with therapy is dissected: while biologics induce drug-specific microbiome shifts that often correlate with clinical normalization, they also carry infection risks that must be strategically managed. Emerging microbiome-targeted interventions like specific probiotics show promise but are hampered by methodological inconsistencies. This review uniquely highlights the causality gap and proposes that future breakthroughs require a shift from correlation to mechanism. We conclude that the microbiome is a dynamic interface between genes and environment in psoriasis; its successful integration into diagnostic and therapeutic paradigms demands standardized multi-omics approaches, functional validation, and personalized medicine strategies that target this critical axis.
Summary
Keywords
causality, gut-skin axis, IL-23/Th17 pathway, Microbiome dysbiosis, Pathogenic Mechanism, Psoriasis, Therapeutic modulation
Received
27 September 2025
Accepted
17 February 2026
Copyright
© 2026 Wang, Zhang, Lin, Wang and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Suqing Yang
Disclaimer
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