The inflammatory origin of psoriasis remains mysterious. Study results showed microbiota changes in these patients.
Psoriasis affects around 2% of the population, at all ages. It is characterized by chronic skin inflammation. It appears in people who are genetically predisposed with physical or psychological factors facilitating its onset. This inflammation leads to uncontrolled proliferation of epidermal cells, with keratinocytes being replaced in 3 days instead of 28, and the cells have anomalies. Moreover, 20% of the patient also have painful joint involvement1.
A disrupted intestinal microbiota
The origin of the inflammation remains unknown, but researchers have detected differences between the intestinal microbiota (gut flora) of healthy subjects, and those of people with psoriasis alone or psoriasis and arthritis. That observation suggests a potential microbiota role in the cutaneous lesions and arthritis onset2.
Different dysbioses in the presence of arthritis
The intestinal microbiota of psoriasis patients is less diverse and less rich in Coprococcus2. In those who also have arthritis, Ruminococcus and Akkermansia muciniphila are less represented, like in patients with chronic inflammatory bowel diseases2. Ongoing research is trying to determine whether the intestinal microbiota anomalies precede arthritis onset, which could help to screen at-risk subjects and might suggest a causal relationship2.
Local and systemic treatments
Depending on its severity, psoriasis is based on topical agents (steroids, vitamin D3 analogues) and phototherapy, or systemic molecules (retinoids, methotrexate, cyclosporine and biopharmaceuticals). Current studies are investigating the impact of probiotics on localized cutaneous inflammation and dysbiosis.
1. Société Française de dermatologie. http://dermato-info.fr/article/Le_psoriasis
2. Scher JU et al. Decreased bacterial diversity characterizes the altered gut microbiota in patients with psoriatic arthritis, resembling dysbiosis in inflammatory bowel disease. Arthritis Rheumatol 2015;67:128-39.