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Review
. 2020 Dec 15:11:589726.
doi: 10.3389/fmicb.2020.589726. eCollection 2020.

Skin and Gut Microbiome in Psoriasis: Gaining Insight Into the Pathophysiology of It and Finding Novel Therapeutic Strategies

Lihui Chen  1   2   3   4   5 , Jie Li  1   4   5 , Wu Zhu  1   4   5 , Yehong Kuang  1   4   5 , Tao Liu  6 , Wei Zhang  2   3 , Xiang Chen  1   4   5 , Cong Peng  1   4   5
Affiliations
Review

Skin and Gut Microbiome in Psoriasis: Gaining Insight Into the Pathophysiology of It and Finding Novel Therapeutic Strategies

Lihui Chen et al. Front Microbiol. .

Abstract

Psoriasis affects the health of myriad populations around the world. The pathogenesis is multifactorial, and the exact driving factor remains unclear. This condition arises from the interaction between hyperproliferative keratinocytes and infiltrating immune cells, with poor prognosis and high recurrence. Better clinical treatments remain to be explored. There is much evidence that alterations in the skin and intestinal microbiome play an important role in the pathogenesis of psoriasis, and restoration of the microbiome is a promising preventive and therapeutic strategy for psoriasis. Herein, we have reviewed recent studies on the psoriasis-related microbiome in an attempt to confidently identify the "core" microbiome of psoriasis patients, understand the role of microbiome in the pathogenesis of psoriasis, and explore new therapeutic strategies for psoriasis through microbial intervention.

Keywords: gut microbiota; immunity; microbial interventions; psoriasis; skin microbiota.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
The putative relationship between gut dysbiosis and psoriasis onset and progression. Intestinal barrier function is maintained by group 3 innate lymphoid cells (ILC3s) and IL-17- and IL-22-producing T helper 17 (Th17) cells, which modulate antimicrobial peptide secretion by intestinal epithelial cells (IECs) and IgA production in the gut (Hirota et al., 2013; Kruglov et al., 2013). Moreover, dendritic cells (DCs) participate in microbiota sensing via the Mincle-Syk axis to regulate IL-17 and IL-22 production and promote intestinal barrier integrity (Martinez-Lopez et al., 2019). Host- and microbiota-derived factors induce gut microbe dysbiosis, including disruption of gut barrier integrity and increased permeability, as well as alterations in microbial metabolites such as SCFAs, secondary bile acids, tryptophan, lipopolysaccharides (LPSs) and phenols, thus disturbing immune homeostasis via a low-grade chronic inflammatory process. For example, the intestinal microbiota promotes psoriasis-like skin inflammation by enhancing the Th17 response, and regulatory T cell (Treg) levels decrease in psoriasis patients, leading to an imbalance between effector T cells and suppressor T cells (Zakostelska et al., 2016; Komine, 2020). Th17 cell differentiation requires IL-6 and transforming growth factor-β (TGF-β) from DCs in an antigen-dependent manner (Ivanov et al., 2006; Persson et al., 2013). In contrast, activation of ILC3s requires the release of IL-23 by myeloid cells to produce IL-22 and/or IL-17, which is antigen dependent (Satpathy et al., 2013; Longman et al., 2014). Increased numbers of ILC3s exist in the circulating blood of psoriatic arthritis patients, as well as the lesional and non-lesional skin of psoriasis patients (Soare et al., 2018). Phenols, as metabolites of aromatic amino acids produced by gut bacteria and regarded as bioactive toxins and serum biomarkers of a disturbed gut environment, have the ability to influence keratinocyte differentiation in the skin, but the underlying mechanism remains to be explored (Miyazaki et al., 2014). The involvement of immune cells and their active factors and intestinal microorganisms and their metabolites promotes the progression of psoriasis.
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