Role of skin and gut microbiota in the pathogenesis of psoriasis, an inflammatory skin disease

Abstract

Psoriasis is a chronic inflammatory skin disease associated with epidermal keratinocyte hyperplasia and epidermal immune cell over-activation. Compositions of both local skin and gut microbiome are linked to modulation of inflammation and disease severity in psoriasis. Owing to the situation that different bacteria may elicit differential immune or inflammatory responses from epidermal immune cells and keratinocytes, and to-date no single pathogen was highlighted to be responsible for psoriasis, disruption of homeostasis (dysbiosis) in the original microbial ecosystems may create a disease-promoting environment, and as a whole may be a primary causal factor. Several studies have provided evidence that the dominant IL-23/IL-17 pathogenesis pathway is regulated by metabolites produced by gut and skin microbiota. This review summarizes the approaches commonly used for functional characterization of the microbiome compositions associated with development of clinical phenotypes of psoriasis. The underlying mechanisms by which microbiota modulate immune cells and keratinocytes are also proposed.