Abstract
There is a known association between psoriasis and Crohn disease (CD). Patients with CD are five times more likely to develop psoriasis, and, conversely, patients with psoriasis are more likely to develop CD.
Many gastroenterologists now accept that CD results from a breakdown of immune tolerance to the microbiota of the intestine in genetically susceptible individuals. The microbiota of the skin have recently been investigated in psoriasis.
Firmicutes was the most common phylum, and Streptococcus the most common genus identified. Beta-haemolytic streptococci have been implicated in both guttate and chronic plaque psoriasis.
Furthermore, the innate immune system has been shown to be activated in psoriasis, and many of the genes associated with the disease are concerned with the signalling pathways of the innate immune system, notably interleukin-23 and nuclear factor κB. Patients with psoriasis also have an increased incidence of periodontitis, a disease thought to be due to an abnormal response to normal oral commensals.
Based on the similarities between CD and psoriasis, we propose that psoriasis is due to a breakdown of immune tolerance to the microbiota of the skin. In support of this hypothesis we provide evidence for microbiota in the skin, activation of the innate immune system, and genetic abnormalities involving the innate immune system.