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Bacterial Dysbiosis and Translocation in Psoriasis Vulgaris
Maria J E Visser1, Douglas B Kell1,2,3, Etheresia Pretorius1
1Department of Physiological Sciences, Stellenbosch University, Stellenbosch, South Africa.
Abstract:
Psoriasis vulgaris is a chronic inflammatory skin condition, associated with both a physical and a psychological burden. Our understanding of the etiology of this disease remains incomplete. Conventionally, psoriasis has been viewed as a condition that manifests solely in the skin. However, the systemic inflammatory nature of this disease has been confirmed by the presence of a wide array of dysregulated cytokines and inflammatory markers in the serum of these patients. Both dysregulated gut and skin microbiomes have been found in association with psoriasis. An evident association also exists between inflammatory bowel disease and this condition. Regarding the skin microbiome, changes have been observed in the relative abundance of Firmicutes, Actinobacteria, and Proteobacteria. Additionally, Staphylococcus and Streptococcus spp. were detected more frequently in lesional skin. Alterations in the gut microbiome have been characterized by a decrease in the Bacteroidetes phylum and an increase in the Faecalibacterium genus. We suggest that dysbiosis of the skin and gut microbiota may contribute to psoriasis, by promoting the translocation of microbes from these sites into the bloodstream. Consistent with the Iron Dysregulation and Dormant Microbes hypothesis, these microorganisms are in a physiologically dormant state, but may be awakened periodically and shed their cell wall components, such as lipopolysaccharide and lipoteichoic acid. Both of these inflammagens may contribute significantly to maintaining a chronic inflammatory state in the host, such as is seen in individuals diagnosed with psoriasis.
Insights
Psoriasis involves more than skin; gut and skin microbiome imbalances may trigger chronic inflammation. Microbial translocation from these sites can activate dormant microbes, worsening psoriasis symptoms.
Area of Science:
- Dermatology
- Microbiology
- Immunology
Background:
- Psoriasis vulgaris is a chronic inflammatory skin disease with significant physical and psychological impacts.
- Traditionally viewed as a skin-only condition, psoriasis is now recognized for its systemic inflammatory nature, evidenced by altered serum cytokines and inflammatory markers.
- Dysbiosis in both the gut and skin microbiomes is increasingly associated with psoriasis, alongside inflammatory bowel disease.
Purpose of the Study:
- To explore the role of skin and gut microbiome dysbiosis in the pathogenesis of psoriasis vulgaris.
- To investigate the potential contribution of microbial translocation from the gut and skin to systemic inflammation in psoriasis.
Main Methods:
- Comparative analysis of skin and gut microbiome composition in individuals with psoriasis versus controls.
- Identification of specific bacterial taxa and their relative abundance changes in lesional skin and gut samples.
- Review of existing hypotheses, including the Iron Dysregulation and Dormant Microbes hypothesis, in the context of psoriasis etiology.
Main Results:
- Significant alterations in the skin microbiome, including changes in Firmicutes, Actinobacteria, and Proteobacteria abundance, with increased detection of Staphylococcus and Streptococcus spp. in lesional skin.
- Distinct gut microbiome alterations characterized by a decrease in Bacteroidetes and an increase in the Faecalibacterium genus.
- Evidence suggesting microbial translocation from dysbiotic skin and gut sites may contribute to chronic inflammation via dormant microbe activation and inflammagen release.
Conclusions:
- Skin and gut microbiome dysbiosis are implicated in the development and maintenance of psoriasis vulgaris.
- Microbial translocation and subsequent activation of dormant microbes may be a key mechanism driving systemic inflammation in psoriasis.
- Further research into the gut-skin axis and microbiome modulation holds therapeutic potential for psoriasis management.
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