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Review
. 2023 Jul 10;13(7):1100.
doi: 10.3390/biom13071100.

Microbiota and IL-33/31 Axis Linkage: Implications and Therapeutic Perspectives in Atopic Dermatitis and Psoriasis

Laura Bonzano  1 , Francesco Borgia  2 , Rossella Casella  3 , Andrea Miniello  3 , Eustachio Nettis  3 , Sebastiano Gangemi  4
Affiliations
Review

Microbiota and IL-33/31 Axis Linkage: Implications and Therapeutic Perspectives in Atopic Dermatitis and Psoriasis

Laura Bonzano et al. Biomolecules. .

Abstract

Microbiome dysbiosis and cytokine alternations are key features of atopic dermatitis (AD) and psoriasis (PsO), two of the most prevalent and burdensome pruritic skin conditions worldwide. Interleukin (IL)-33 and IL-31 have been recognized to be major players who act synergistically in the pathogenesis and maintenance of different chronic inflammatory conditions and pruritic skin disorders, including AD and PsO, and their potential role as therapeutic targets is being thoroughly investigated. The bidirectional interplay between dysbiosis and immunological changes has been extensively studied, but there is still debate regarding which of these two factors is the actual causative culprit behind the aetiopathological process that ultimately leads to AD and PsO. We conducted a literature review on the Pubmed database assessing articles of immunology, dermatology, microbiology and allergology with the aim to strengthen the hypothesis that dysbiosis is at the origin of the IL-33/IL-31 dysregulation that contributes to the pathogenesis of AD and PsO. Finally, we discussed the therapeutic options currently in development for the treatment of these skin conditions targeting IL-31, IL-33 and/or the microbiome.

Keywords: IL-31; IL-33; atopic dermatitis; cytokines; inflammation; microbiota; pathogenesis; psoriasis; skin; treatment.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The difference between healthy skin (A) and atopic dermatitis (B). In picture (B), the role of S. Aureus in eliciting the production of IL-33 by keratinocytes is represented. Further, gut dysbiosis (C) also induces the inflammatory pathway.
Figure 2
Figure 2
The role of gut and skin dysbiosis and the IL-33/31 axis in inducing psoriatic lesions.
See this image and copyright information in PMC

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