Dysbiosis of gut microbiota and its correlation with dysregulation of cytokines in psoriasis patients

Abstract

Background Psoriasis is an inflammatory skin disease associated with multiple comorbidities and substantially diminishes patients’ quality of life. The gut microbiome has become a hot topic in psoriasis as it has been shown to affect both allergy and autoimmunity diseases in recent studies. Our objective was to identify differences in the fecal microbial composition of patients with psoriasis compared with healthy individuals to unravel the microbiota profiling in this autoimmune disease. Results We collected fecal samples from 30 psoriasis patients and 30 healthy controls, sequenced them by 16S rRNA high-throughput sequencing, and identified the gut microbial composition using bioinformatic analyses including Quantitative Insights into Microbial Ecology (QIIME) and Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt). Our results showed that different relative abundance of certain bacterial taxa between psoriasis patients and healthy individuals, including Faecalibacterium and Megamonas, were increased in patients with psoriasis. It’s also implicated that many cytokines act as main effect molecules in the pathology of psoriasis. We selected the inflammation-related indicators that were abnormal in psoriasis patients and found the microbiome variations were associated with the level of them, especially interleukin-2 receptor showed a positive relationship with Phascolarctobacterium and a negative relationship with the Dialister. The relative abundance of Phascolarctobacterium and Dialister can be regard as predictors of psoriasis activity. The correlation analysis based on microbiota and Inflammation-related indicators showed that microbiota dysbiosis might induce an abnormal immune response in psoriasis. Conclusions We concluded that the gut microbiome composition in psoriasis patients has been altered markedly and provides evidence to understand the relationship between gut microbiota and psoriasis. More mechanistic experiments are needed to determine whether the differences observed in gut microbiota are the cause or consequences of psoriasis and whether the relationship between gut microbiota and cytokines was involved.

Intestinal Dysbiosis Exacerbates the Pathogenesis of Psoriasis-Like Phenotype Through Changes in Fatty Acid Metabolism

“…It has been reported that, compared with healthy patients, the abundance of Prevotella in the intestines of patients with psoriasis is increased, while that of the Porphyromonadaceae family, to which Parabacteroides distasonis belongs, is decreased (32,33). Thus, our ndings suggest that the intestinal microbiota plays an important role in the progression of psoriasis.…”

Involvement of Gut Microbiota in the Development of Psoriasis Vulgaris

“…Later, we found the recovery process of patients with psoriasis was accompanied by reduction of certain "psoriatic characteristic bacterial genera" (13,15,16,33), which had been identified by published studies comparing gut bacteria in patients with psoriasis and healthy controls. Specific bacterial differences at all levels of taxonomic classification were summarized in Supplementary Table 9 (13)(14)(15)(16)(17)(18)(33)(34)(35)(36)(37)(38)(39). The F/B ratio has been shown to be significantly related to certain psoriasis comorbidities (e.g., metabolic syndrome) and be positively correlated with PASI score by comparison of gut metagenome between patients with psoriasis and healthy people (15,37).…”

Skin Barrier Dysregulation in Psoriasis

“…Microbiota produce short and medium chain fatty acids which can regulate immune responses, which may explain their link to psoriasis pathogenesis [ 204 ]. For example, alterations in the gut microbiome correlate with increases in inflammatory markers, including the IL-2 receptor and the complement 3 protein [ 205 ]. Additionally, the gut microbiome from psoriasis patients has a lower gene expression of proteins which synthesise butyrate (an anti-inflammatory short-chain fatty acid) than healthy controls [ 206 , 207 ].…”