Gut Microbiota in Psoriasis: Evidence for Dysbiosis, Pathological Mechanisms, Causality, and Therapeutic Implications

Abstract

Psoriasis is a chronic inflammatory skin disease driven by genetic susceptibility, environmental triggers, and immune dysregulation, with a global prevalence of approximately 2%–3%. In recent years, the gut microbiota has garnered increasing attention as a key interface linking environmental factors to host immunity in the pathogenesis of psoriasis. A growing body of research has revealed significant gut dysbiosis in patients with psoriasis, characterized by reduced microbial diversity, depletion of specific beneficial bacteria, and enrichment of opportunistic pathogens. Mechanistically, the gut microbiota participates in the pathological process of psoriasis through modulation of the Th17/IL-23 axis, induction of regulatory T cell dysfunction, disruption of the intestinal barrier leading to bacterial translocation, and imbalance of microbial metabolites. Regarding causal evidence, germ-free animal models, fecal microbiota transplantation experiments, and Mendelian randomization studies have provided multi-level support for causal relationships between specific microbial taxa and psoriasis. Therapeutically, microbiota-targeting strategies including probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation have shown potential to ameliorate psoriasis severity in preclinical and preliminary clinical studies. This review systematically synthesizes the above evidence, delineates the characteristics of dysbiosis, pathological mechanisms, the causal evidence chain, and therapeutic translation prospects, and highlights current limitations and future directions.

Introduction

Psoriasis is an immune-mediated chronic recurrent inflammatory disease characterized by excessive proliferation and abnormal differentiation of keratinocytes. Its clinical manifestations include well-demarcated erythematous, scaly plaques, and it may involve the joints (psoriatic arthritis) and be accompanied by multiple comorbidities including cardiovascular disease, metabolic syndrome, and inflammatory bowel disease. Its pathogenesis has long been considered a T cell–mediated autoinflammatory response triggered by environmental factors against a background of genetic susceptibility, with the IL-23/Th17 axis occupying a central position.^1,2

However, genetic factors only partially explain disease susceptibility. Genome-wide association studies (GWAS) have identified that the genetic loci significantly associated with psoriasis are predominantly located in immune pathways, yet the concordance rate of psoriasis in monozygotic twins is only approximately 35%–70%, suggesting that environmental factors play a non-negligible role in disease development.³ Among the various environmental factors, the microbiota—particularly the gut microbiota—has emerged in recent years as a potential key link connecting genetic susceptibility to immune dysregulation.

The human gut harbors approximately 10¹³–10¹⁴ microorganisms, with a collective genetic repertoire approximately 150 times larger than the human genome. The gut microbiota plays indispensable roles in immune system development, metabolic homeostasis, and maintenance of barrier function. Gut microbial dysbiosis has been extensively linked to a variety of immune-mediated diseases, including inflammatory bowel disease, rheumatoid arthritis, and type 1 diabetes, and the concept of the “gut–skin axis” in the field of dermatology has gradually gained experimental support.^4,5

This review aims to systematically synthesize the evidence for gut microbiota dysbiosis in psoriasis, the underlying pathological mechanisms, the causal evidence, and the latest advances in microbiota-targeting therapies, with a focus on high-quality studies published in the past five years (2020–2025), thereby providing a comprehensive perspective for understanding the pathogenesis of psoriasis and exploring novel therapeutic strategies.

Evidence for Gut Microbiota Dysbiosis in Patients with Psoriasis

Changes in Microbial Diversity

Multiple 16S rRNA gene sequencing and metagenomic studies have consistently reported that the α-diversity (within-sample diversity) of the gut microbiota in patients with psoriasis is significantly lower than that in healthy controls. Scher et al found in a study of patients with psoriatic arthritis that both the Shannon diversity and phylogenetic diversity of the gut microbiota were reduced.⁶ In recent years, several larger-scale studies have replicated and extended this finding. A systematic review and meta-analysis published in 2022 that pooled data from multiple case–control studies confirmed that both the Shannon index and Chao1 index of the gut microbiota in patients with psoriasis were significantly lower than those in healthy controls, and this difference remained robust after excluding patients who had received systemic immunosuppressive therapy.⁷

β-diversity analyses have also demonstrated significant separation in community structure between patients and healthy controls. Multiple studies using principal coordinate analysis (PCoA) and PERMANOVA testing have confirmed that the overall gut microbiota structure in patients with psoriasis differs significantly from that of healthy individuals^7,8. It is worth noting that not all studies have observed consistent reductions in diversity. A minority of studies (eg, Dei-Cas et al, 2020) reported no significant difference in α-diversity between psoriasis patients and controls, which may be attributable to limited sample size, differences in disease activity, and insufficient sequencing depth.⁸ Overall, however, the majority of recent large-sample studies tend to support a reduction in gut microbiota diversity in patients with psoriasis, with the degree of reduction correlating with disease severity.

Changes in the Abundance of Specific Microbial Taxa

At the phylum level, the gut microbiota of patients with psoriasis typically exhibits alterations in the Firmicutes/Bacteroidetes ratio, although the direction is not entirely consistent across studies. Some studies have reported an increase in the relative abundance of Firmicutes and a decrease in Bacteroidetes, while others have reported opposite findings, suggesting that coarse-grained changes at the phylum level may obscure functionally relevant changes at the genus and species levels.

At the genus and species levels, studies from the past five years have further consolidated the following relatively consistent trends:

Depleted Taxa

• Akkermansia muciniphila: Multiple studies have consistently reported a significant reduction in the abundance of this bacterium in the gut of patients with psoriasis. A. muciniphila is a mucin-degrading bacterium closely associated with intestinal barrier integrity and metabolic health. A systematic review and meta-analysis confirmed that the relative abundance of A. muciniphila in patients with psoriasis is significantly lower than that in controls⁷. The reduction of this bacterium may promote increased intestinal permeability, which is associated with the systemic inflammatory state of the disease.

• Faecalibacterium prausnitzii: As an important butyrate-producing bacterium and anti-inflammatory commensal, F. prausnitzii is consistently reduced in patients with psoriasis. Multiple studies have reported that its abundance is negatively correlated with the PASI score⁹. Shapiro et al found that the abundance of F. prausnitzii significantly recovered in patients who responded well to biologic therapy, suggesting its potential as a biomarker of treatment response.¹⁰

• Roseburia and Eubacterium rectale: Both are butyrate-producing bacteria that have also been reported to be reduced in patients with psoriasis.⁹

• Various probiotic strains within the genera Bifidobacterium and Lactobacillus are reduced in patients with psoriasis, with the reduction being particularly pronounced in pediatric psoriasis patients.¹¹

Enriched Taxa

• Escherichia coli and various members of the Enterobacteriaceae family are enriched in patients with psoriasis, some strains of which may exert their effects through the production of inflammatory molecules such as lipopolysaccharide (LPS). This trend has been reported in multiple metagenomic studies.¹²

• Opportunistic pathogens such as Streptococcus and Enterococcus are increased in abundance.^7,9

• Ruminococcus gnavus is enriched in patients with psoriatic arthritis, and this bacterium is associated with multiple inflammatory diseases.¹²

• Klebsiella has been reported to be increased in some studies, particularly in psoriasis patients with concomitant metabolic syndrome.⁹

Functional Dysbiosis

Metagenomic and metabolomic analyses have revealed a functional shift in the gut microbiota of patients with psoriasis. Compared with healthy controls, the gut metagenome of patients shows enrichment of genes involved in lipopolysaccharide biosynthesis, branched-chain amino acid metabolism, and tryptophan degradation, while genes involved in short-chain fatty acid (SCFA) synthesis (particularly butyrate synthesis) are relatively reduced¹². Fecal metabolomic studies have also shown that fecal levels of SCFAs (acetate, propionate, and butyrate) are decreased in patients with psoriasis, indole metabolites are reduced, while trimethylamine-N-oxide (TMAO) and certain secondary bile acid metabolites are elevated¹³. These functional alterations corroborate the compositional changes in the microbiota and collectively constitute the multi-dimensional evidence for gut microbiota dysbiosis in psoriasis.

Pathological Mechanisms: How the Gut Microbiota Drives Psoriasis

Microbiota-Dependent Activation of the Th17/IL-23 Axis

The core immune abnormality in psoriasis is the hyperactivation of the IL-23/Th17 axis. IL-23, produced by dendritic cells and macrophages, promotes the differentiation and expansion of Th17 cells, which subsequently secrete cytokines such as IL-17A, IL-17F, and IL-22, driving excessive keratinocyte proliferation and the formation of an inflammatory microenvironment^1,2. The gut microbiota modulates this axis at multiple levels.

First, segmented filamentous bacteria (SFB) are among the most potent known inducers of intestinal Th17 cells. SFB strongly induce Th17 cell differentiation in the intestinal lamina propria by adhering to intestinal epithelial cells and activating a serum amyloid A (SAA)-dependent pathway. Although SFB colonization in the human gut is less prevalent than in mice, bacteria with similar functions (such as certain strains of Bifidobacterium adolescentis and adherent E. coli) may play analogous roles¹⁴. Zákostelská et al found that germ-free mice had a severe deficiency of intestinal Th17 cells, and that transplantation of fecal microbiota from patients with psoriasis enhanced both intestinal and cutaneous Th17 responses, demonstrating that psoriasis-associated microbiota possess the capacity to induce Th17 polarization¹⁵. Recent studies have further elucidated the molecular mechanisms by which the microbiota induces Th17 cells. Microbiota-derived ATP and SAA act on intestinal dendritic cells and innate lymphoid cells to create an IL-1β/IL-23-enriched microenvironment, thereby promoting the stable differentiation of Th17 cells^14,16. In addition, certain gut commensals may activate skin-homing Th17 cells through cross-reactive T cell receptors, which may explain how gut dysbiosis affects distal cutaneous immune responses.¹⁶

Second, the loss of immunomodulatory effects of short-chain fatty acids represents another important mechanism. SCFAs (particularly butyrate) promote the differentiation and function of Foxp3+ regulatory T cells (Tregs) by inhibiting histone deacetylases (HDACs) and suppress the NF-κB pathway through receptors such as GPR43 and GPR109A, exerting systemic anti-inflammatory effects¹⁷. The reduction of butyrate-producing bacteria (such as F. prausnitzii, Roseburia, and E. rectale) in patients with psoriasis leads to decreased SCFA levels, which may shift the Treg/Th17 balance toward a pro-inflammatory state. In vitro experiments have confirmed that butyrate inhibits Th17 cell differentiation and promotes Treg generation¹⁷. Multiple studies in imiquimod (IMQ)-induced psoriasis-like mouse models have demonstrated that oral administration of sodium butyrate or tributyrin significantly reduces cutaneous IL-17A expression and epidermal thickness while increasing the proportion of Foxp3+ Tregs in the spleen and intestinal lamina propria, further validating the in vivo protective effects of SCFAs.^17,18

Intestinal Barrier Dysfunction and Bacterial Translocation

Gut microbiota dysbiosis can compromise the integrity of the intestinal barrier. The reduction of A. muciniphila impairs the normal renewal and maintenance of the mucus layer; insufficient SCFAs reduce the expression of tight junction proteins (such as occludin, claudin-1, and ZO-1) between intestinal epithelial cells; and LPS from pro-inflammatory bacteria promotes intestinal epithelial cell apoptosis and increases paracellular permeability through TLR4/MyD88/NF-κB signaling¹⁹. Together, these changes lead to a “leaky gut” state.

Increased intestinal permeability allows bacteria and their components (LPS, peptidoglycan, and bacterial DNA) to enter the systemic circulation and distant tissues via the portal vein. In patients with psoriasis, multiple studies have detected elevated plasma LPS levels and anti-LPS antibody titers that correlate with disease severity. Sikora et al summarized the evidence for intestinal barrier dysfunction in psoriasis in a systematic review, noting that patients exhibit significantly elevated plasma LPS concentrations and intestinal permeability markers (such as zonulin) that positively correlate with the PASI score¹⁹. The detection rate of circulating microbial DNA in the blood of patients with psoriasis is also higher than that in healthy individuals. Ramírez-Boscá et al first reported a significantly increased rate of bacterial DNA positivity in the blood of psoriasis patients, and recent studies using more sensitive molecular techniques have further confirmed this finding.²⁰ These microbe-associated molecular patterns (MAMPs) activate TLRs on macrophages, dendritic cells, and keratinocytes in the skin, promoting local inflammatory responses and forming the distal “leaky gut–skin inflammation” effector pathway.¹⁹

Molecular Mimicry and Autoreactivity

Molecular mimicry between the gut microbiota and host antigens may contribute to the generation of autoimmune-like responses in psoriasis. A well-recognized example is the sequence homology between streptococcal M protein and keratin. The association between psoriasis and streptococcal infection has long been established by clinical observations (particularly in guttate psoriasis), and the enrichment of intestinal Streptococcus may persistently activate autoreactive T cells through similar cross-reactive mechanisms.²¹ Ruiz-Romeu et al demonstrated that CD8⁺ T cells in the skin of patients with psoriasis can recognize streptococcal M protein peptides with sequence homology to keratin 17, and that this cross-recognition is dependent on HLA-C*06:02, the strongest genetic risk allele for psoriasis.²² This provides molecular-level evidence for the tripartite interaction of “microbiota–genetics–immunity”.

In addition, MAM protein (mycoplasma arthritidis mitogen)-like superantigens and certain heat shock proteins derived from the gut microbiota have also been suggested to potentially trigger or amplify immune responses against cutaneous self-antigens.²¹ Although these findings primarily derive from studies of cutaneous Streptococcus, the enriched Streptococcus populations in the gut may act through the same molecular mimicry mechanisms, and their specific contributions await further validation.

Tryptophan Metabolism and Aryl Hydrocarbon Receptor Signaling

The gut microbiota metabolizes tryptophan to produce various indole derivatives (such as indole-3-acetic acid, indole-3-propionic acid, and indole-3-aldehyde), which are natural ligands of the aryl hydrocarbon receptor (AhR). AhR plays important roles in maintaining intestinal immune homeostasis and skin barrier function. The reduction of tryptophan metabolism genes in the gut microbiota of patients with psoriasis leads to insufficient AhR ligands, which may weaken AhR-mediated anti-inflammatory signaling and the regulation of IL-22.^12,13 In IMQ-induced mouse models, supplementation with indole-3-aldehyde or lactobacillus strains with tryptophan-metabolizing capacity activates AhR signaling and alleviates skin inflammation, suggesting that tryptophan metabolites may constitute another important channel through which the gut microbiota regulates cutaneous immunity.²³

Causal Evidence

Germ-Free Animal Models and Fecal Microbiota Transplantation Experiments

The most compelling evidence for causal inference comes from germ-free animal models and fecal microbiota transplantation (FMT) experiments. The landmark study by Zákostelská et al first demonstrated that transplantation of fecal microbiota from patients with psoriasis into germ-free mice significantly increased susceptibility to IMQ-induced psoriasis-like skin inflammation, manifesting as aggravated epidermal thickening and elevated expression of IL-17A and IL-22.¹⁵ Stehlikova et al further found that mice receiving psoriasis patient microbiota not only exhibited aggravated skin inflammation but also developed impaired intestinal barrier function and elevated systemic inflammatory markers, suggesting that microbiota transplantation alone is sufficient to recapitulate disease-associated immune phenotypes in recipient mice.²⁴

In recent years, more studies have established causal links between specific microbial taxa and psoriasis phenotypes through microbiota transplantation experiments. Zhao et al transplanted fecal microbiota from patients with psoriasis and healthy controls separately into mice whose gut microbiota had been depleted by antibiotics, and found that mice receiving psoriasis patient microbiota exhibited more severe skin inflammation, higher cutaneous IL-17A expression, and lower intestinal Treg proportions following IMQ stimulation. More importantly, through “add-back experiments” combining FMT with supplementation of specific bacterial strains, the study demonstrated that supplementing F. prausnitzii or A. muciniphila back into mice receiving psoriasis patient microbiota significantly alleviated skin inflammation, providing direct evidence for the protective causal roles of these beneficial bacteria.¹²

Mendelian Randomization Studies

Mendelian randomization (MR) uses genetic variants as instrumental variables to assess causal associations between exposures and outcomes, effectively avoiding confounding factors and reverse causation issues inherent in observational studies. In recent years, multiple MR studies have investigated the causal relationships between the gut microbiota and psoriasis.

Liu et al conducted a two-sample MR analysis using gut microbiota GWAS summary data from the MiBioGen consortium (covering 211 bacterial genera) and psoriasis GWAS data, and identified significant causal associations between multiple bacterial genera and psoriasis risk. Specifically, increases in the genera Ruminococcus and Eubacterium fissicatena were associated with elevated psoriasis risk, while increases in Butyricicoccus and Coprococcus were associated with reduced risk²⁵. Sensitivity analyses in this study (including weighted median, MR-Egger regression, and leave-one-out analyses) supported the robustness of the findings.

Another MR study published in 2024 using updated psoriasis GWAS data from the FinnGen consortium confirmed that the genetically predicted abundance of the genus Faecalibacterium was negatively associated with psoriasis risk, while Streptococcus was positively associated with risk.²⁶ Furthermore, reverse MR analysis did not identify significant causal effects of psoriasis genetic susceptibility on gut microbiota composition, supporting a causal direction of “microbiota → disease” rather than the reverse. However, it should be noted that the interpretation of MR results is constrained by the strength of the instrumental variables, potential horizontal pleiotropy, and the taxonomic resolution of the gut microbiota GWAS data, and should therefore be considered in conjunction with other lines of evidence.

Longitudinal Studies and Evidence from Therapeutic Interventions

Changes in the gut microbiota before and after biologic therapy provide another form of causal support. Multiple longitudinal studies have tracked the dynamic changes in the gut microbiota of patients with psoriasis receiving treatment with IL-17 inhibitors (such as secukinumab), IL-23 inhibitors (such as guselkumab), or TNF-α inhibitors. Shapiro et al longitudinally followed psoriasis patients receiving biologic therapy and found that responders exhibited significant recovery of gut microbiota α-diversity, increased abundance of F. prausnitzii and A. muciniphila, and decreased abundance of pro-inflammatory taxa¹⁰. Another study that followed patients with moderate-to-severe psoriasis receiving secukinumab therapy for 24 weeks observed similar microbiota recovery trends, with the degree of microbiota recovery correlating with the degree of PASI improvement.²⁷ These data suggest that effective control of skin inflammation may indirectly promote gut microbiota recovery, or that biologics may indirectly modulate the gut microbiota by altering the systemic immune environment; the causal sequence between the two requires further elucidation.

Therapeutic Implications: Microbiota-Targeting Intervention Strategies

Probiotics and Prebiotics

Probiotics represent one of the most feasible microbiota-targeting intervention approaches. Multiple randomized controlled trials (RCTs) have evaluated the efficacy of probiotics as adjunctive therapy for psoriasis.

Navarro-López et al conducted a randomized, double-blind, placebo-controlled trial in which 90 patients with plaque psoriasis received an oral probiotic mixture (containing Bifidobacterium longum, B. lactis and Lactobacillus rhamnosus) or placebo for 12 weeks. The results showed that the reduction in PASI score in the probiotic group was significantly greater than that in the placebo group, with a lower recurrence rate.²⁸ Moludi et al evaluated a probiotic preparation containing multiple Lactobacillus and Bifidobacterium strains as adjunctive therapy in patients with psoriasis and found that after 12 weeks of intervention, the probiotic group showed significant improvements in PASI score and serum inflammatory markers (hs-CRP).²⁹ The early proof-of-concept study by Groeger et al also supported the potential benefits of probiotics in psoriasis³⁰. A systematic review and meta-analysis published in 2024 that pooled evidence from multiple RCTs concluded that probiotic adjunctive therapy significantly reduces PASI scores, although the inter-study heterogeneity was substantial and the evidence grade was moderate.³¹

Regarding prebiotics, dietary fibers such as fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS), and inulin that selectively promote the growth of bifidobacteria and lactobacilli have shown potential benefits. Kanda et al found in an IMQ-induced mouse model that prebiotic supplementation promoted the growth of beneficial gut bacteria, increased fecal SCFA levels, and alleviated skin inflammation and IL-17 expression¹⁸. However, clinical RCTs of prebiotics in patients with psoriasis remain scarce, and the current evidence derives mainly from animal experiments and small open-label studies.

Fecal Microbiota Transplantation

Fecal microbiota transplantation (FMT) achieves the reconstruction of the gut microbial ecosystem by transplanting the complete gut microbiota from healthy donors into patients. In the field of psoriasis, the clinical evidence for FMT is still at an early stage, but preliminary results are encouraging.

Komine et al summarized the existing evidence for FMT as a potential therapeutic option for psoriasis in a review, noting that preliminary clinical observations suggest FMT can improve skin lesions in some patients and that gut microbiota diversity increases after transplantation, although rigorous RCTs are still lacking.³² Several registered randomized controlled trials are currently evaluating the efficacy of FMT in psoriasis, and their results will provide a more solid evidence base for this strategy.

Dietary Interventions

Diet is one of the most important environmental factors shaping the composition of the gut microbiota. Observational studies indicate that dietary patterns in patients with psoriasis correlate with disease severity: a high-fat, high-sugar “Western diet” is associated with higher PASI scores and more severe gut dysbiosis, while a Mediterranean diet rich in dietary fiber, polyphenols, and ω-3 polyunsaturated fatty acids is associated with a milder disease phenotype.³³

Regarding interventional studies, Phan et al found in an analysis based on the NutriNet-Santé cohort that Mediterranean diet adherence was negatively associated with psoriasis severity³⁴. A recent review systematically evaluated the existing evidence for dietary interventions in the management of psoriasis, concluding that dietary modification as an adjunctive approach is rational and offers preliminary clinical benefit, but that more high-quality RCTs are needed for confirmation.³³ Although these findings support the adjunctive value of dietary interventions in psoriasis management, the existing studies generally have small sample sizes, short follow-up periods, and difficulties in assessing dietary adherence.

Postbiotics and Microbial Metabolites

Postbiotics refer to inactivated microbial cells or their metabolic products, which offer advantages of high safety and stability. Butyrate, as one of the most extensively studied microbial metabolites, has had its anti-psoriatic potential validated at multiple levels. Several studies have systematically evaluated the therapeutic effects of oral butyrate in IMQ mouse models, finding that butyrate dose-dependently reduces epidermal hyperplasia, lowers cutaneous IL-17A and IL-23 expression, and restores the Treg/Th17 balance.^17,18 In addition, butyrate directly promotes keratinocyte differentiation and inhibits their excessive proliferation by activating the GPR109A receptor on cutaneous keratinocytes.¹⁷

The therapeutic potential of other microbial metabolites is also being explored. Indole-3-aldehyde (an AhR ligand) has shown efficacy in alleviating psoriasis-like inflammation in preclinical models²³. Secondary bile acid metabolites such as ursodeoxycholic acid (UDCA) have shown immunomodulatory effects on the skin and amelioration of psoriasis-like lesions in preliminary studies³⁵. These findings provide a rationale for developing “postbiotic” drugs based on microbiota metabolic mechanisms.

Current Limitations and Future Directions

Despite the substantial progress in research on the gut microbiota in psoriasis, the field still faces numerous challenges:

Methodological Heterogeneity

Studies differ significantly in sample collection methods, DNA extraction protocols, sequencing platforms, bioinformatics pipelines, and statistical approaches, limiting the comparability of results. Establishing standardized research protocols and shared data analysis pipelines is an urgent priority.

Insufficient Control of Confounding Factors

Diet, medications (especially antibiotics and biologics), BMI, and comorbid conditions profoundly influence the gut microbiota, and most cross-sectional studies have inadequately adjusted for these factors. Larger prospective cohort studies employing multivariate adjustment strategies are needed in the future.

Causal Inference Requires Strengthening

Current causal evidence derives primarily from animal models and MR studies, each of which has limitations. Animal models cannot fully recapitulate the complexity of the human microbiota, and MR studies are constrained by instrumental variable strength and taxonomic resolution. Future causal inference should integrate multi-omics data, longitudinal designs, and computational causal inference methods (such as mediation analysis and g-computation).

Insufficient Mechanistic Depth

The current understanding of “how the microbiota remotely influences skin immunity” remains largely descriptive in terms of correlations, and the specific molecular pathways and cellular mediators involved require more in-depth experimental validation. Single-cell sequencing, spatial transcriptomics, and in vivo tracing of microbial metabolites may provide new tools for mechanistic studies.

Challenges in Translational Application

Clinical studies of probiotics and FMT are small in scale and highly heterogeneous, lacking unified product standards and dosing regimens. Donor screening, preparation standardization, and long-term safety monitoring for FMT are key issues that need to be addressed. Furthermore, the optimal timing of microbiota interventions (early intervention vs adjunctive therapy), the applicable patient subgroups (such as those with specific microbiota profiles), and combination strategies (with biologics or phototherapy) all warrant exploration.

Prospects for Personalized Therapy

In the future, stratifying patients based on their gut microbiota profiles to achieve “precision microbiome therapy” is a promising direction. For example, patients with low baseline F. prausnitzii abundance may respond better to probiotic or FMT therapy, while patients with E. coli enrichment may benefit from targeted antimicrobial strategies. This concept needs to be validated through prospective biomarker-driven clinical trials.

Conclusion

Research over the past five years has greatly enriched our understanding of gut microbiota dysbiosis in psoriasis. The evidence consistently demonstrates that patients with psoriasis exhibit reduced gut microbiota diversity, accompanied by depletion of beneficial bacteria such as F. prausnitzii and A. muciniphila and enrichment of potentially pathogenic bacteria such as E. coli and Streptococcus. Mechanistically, gut dysbiosis participates in the aberrant activation of the Th17/IL-23 axis through the attenuation of SCFA-mediated immunoregulation, enhanced intestinal barrier permeability facilitating bacterial translocation, and possible molecular mimicry mechanisms. Multi-level evidence from germ-free animal transplantation experiments, Mendelian randomization studies, and longitudinal observations before and after treatment supports a causal relationship between the gut microbiota and psoriasis. Therapeutically, strategies including probiotics, dietary interventions, and fecal microbiota transplantation have shown potential to improve disease severity in preliminary studies, but require validation through large-scale, standardized clinical trials.

Looking ahead, with advances in multi-omics technologies, causal inference methods, and precision medicine concepts, the gut microbiota holds promise as a new dimension for the auxiliary diagnosis, prognostic assessment, and therapeutic targeting of psoriasis. Integrating microbiome-based interventions into the comprehensive management strategy for psoriasis may offer patients novel benefits beyond conventional immunosuppressive therapy.

Funding Statement

This work was supported by the Science and Technology Research Program of Chongqing Municipal Education Commission (Grant No. KJQN202301132].

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Disclosure

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