- Evidenze sempre maggiori mostrano un’alterazione del microbiota intestinale nei pazienti affetti da patologie autoimmuni.
- Tuttavia, i risultati nei pazienti affetti da psoriasi sono contraddittori e sono basati sul sequenziamento del gene 16S rRNA.
- Il presente studio caso-controllo ha evidenziato differenze nella composizione e nella funzionalità del microbiota intestinale tra i pazienti affetti da psoriasi e i controlli sani.
Abstract
Background
Accumulating evidence supports the findings of an altered gut microbiota in patients with autoimmune disease. However, existing studies on the role of the gut microbiota in patients with psoriasis have demonstrated conflicting results and have mainly been based on 16s rRNA gene sequencing analysis.
Objectives
To examine whether the gut microbiota of patients with psoriasis was altered in composition and functional potentials compared with healthy controls, and as a second approach compared with healthy cohabitant partners. A further aim was to investigate relationships to disease severity, and seasonal impact on the gut microbiota.
Methods
In a case-control study, 126 faecal samples were collected from a sample of 53 systemically untreated patients with plaque psoriasis; 52 healthy controls matched for age, sex and body mass index; and 21 cohabitant partners. A subpopulation of 18 patients with psoriasis and 19 healthy controls continued in a longitudinal study, where four to six faecal samples were collected over 9-12 months. The gut microbiota was characterized using shotgun metagenomic sequencing analysis.
Results
A significantly lower richness (p = 0.007) and difference in community composition (p = 0.01) of metagenomic species was seen in patients with psoriasis compared with healthy controls, and patients with psoriasis had a lower microbial diversity than their partners (p = 0.04). Additionally, the functional richness was decreased in patients with psoriasis compared with healthy controls (p = 0.01) and partners (p = 0.05). Increased disease severity was correlated with alterations in taxonomy and function, with a slight tendency towards a lower richness of metagenomic species, albeit not significant (p = 0.08). The seasonal analysis showed no shifts in community composition in healthy controls or in patients with psoriasis.
Conclusions
The findings of a different gut microbiota in composition and functional potentials between patients with psoriasis and healthy controls support a linkage between the gut microbiota and psoriasis. These findings need to be validated in larger studies, and a potential causal relationship between the gut microbiota and psoriasis still needs to be shown.