Psoriatic patients have a distinct structural and functional fecal microbiota compared with controlsOriginal paper
What was studied?
This multicenter observational study characterized the gut microbial signature of active psoriasis and linked it to predicted metabolic pathways. Researchers compared psoriatic patients with carefully matched non-psoriatic controls. Fecal samples were processed and the 16S rRNA gene was sequenced. Beta-diversity and taxon-level differences were assessed. PICRUSt was used to infer metabolic pathway differences from the 16S data between the two groups.
Who was studied?
The study included 46 participants in Israel, of whom 24 (52 percent) had psoriasis and 22 were controls. Controls were matched for age, body mass index, and comorbidities. Patients had clinically active psoriasis at the time of sampling. Samples were human stool. Matching on body mass index and comorbidities was intended to reduce confounding from metabolic and inflammatory factors known to affect the gut microbiome.
What were the most important findings?
Beta-diversity differed significantly between psoriatic patients and controls, and patients showed a unique genus-level composition. At the phylum level, Firmicutes and Actinobacteria were significantly increased in psoriasis. At the species level, Ruminococcus gnavus, Dorea formicigenerans, and Collinsella aerofaciens were significantly increased (false discovery rate below 0.05). Prevotella copri and Parabacteroides distasonis were significantly decreased. PICRUSt analysis showed increased pathways related to lipopolysaccharide function in the psoriatic cohort.
What are the greatest implications of this study?
The results define a distinct fecal microbial and metabolic signature in active psoriasis, consistent with the gut's proposed role in immune-mediated inflammatory disease. Shifts toward proinflammatory, lipopolysaccharide-related pathways may connect gut bacteria to skin inflammation. Taxa such as Ruminococcus gnavus and Prevotella copri emerge as candidates for further study. The design is cross-sectional and modest in size, so it cannot establish whether dysbiosis drives psoriasis or follows from it.