The skin microbiome as a key regulator of psoriasis: From dysbiotic drivers to host-directed therapeutics.

The skin harbors diverse microbial communities. Compared with gut microbiome dysbiosis, perturbations in the skin microbiome may be more directly implicated in the onset and progression of psoriasis (PSO). More than twenty studies reveal microbial dysbiosis within psoriatic lesions, which is manifested by elevated abundances of pro-inflammatory taxa such as Corynebacterium and Staphylococcus aureus, declined levels of commensal microbes including Cutibacterium, increased total bacterial load and decreased microbial community diversity. Such cutaneous microbial dysbiosis accelerates disease progression via multiple biological pathways, involving impairment of the skin barrier, dysregulation of the innate and adaptive immunity, as well as multifaceted biological effects mediated by microbial metabolites. Microbiome-based diagnostic strategies have emerged as novel tools for evaluating disease prognosis, and targeted modulation of the skin microbiome holds promising prospects for clinical translation. In-depth exploration of skin microbial signatures in PSO enables the skin microbiome to serve as clinically valuable biomarkers for predicting subtype transformation and disease progression and fluctuation. Future research priorities lie in the integration of multi-omics strategies to dissect the potential causal mechanisms underlying host-microbe crosstalk, establish optimized bioengineering techniques and further promote the advancement of individualized therapeutic regimens. Collectively, the skin microbiome not only sheds new light on the pathogenic mechanisms of PSO, but also identifies promising candidate targets for auxiliary diagnosis and precise microbiome-based therapeutic interventions.