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Review
. 2023 Jul;8(3):118-123.
doi: 10.1177/24755303231177965. Epub 2023 Jun 16.

The Emerging Potential of Bile Acids as a Modulator of Psoriatic Inflammation

Affiliations
Review

The Emerging Potential of Bile Acids as a Modulator of Psoriatic Inflammation

Grace Wei et al. J Psoriasis Psoriatic Arthritis. 2023 Jul.

Abstract

Background: Bile acids (BAs) are cholesterol-based amphipathic surfactants that are most widely known for their contributions to lipid metabolism, but more recently have been increasingly recognized as a key signaling molecule in inflammatory diseases as well as, potentially, psoriatic disease.

Objective: This brief review reviews relevant literature in order to briefly describe the synthesis of bile acids and their subsequent metabolism and to analyze recent animal and human data that supports anti-inflammatory activity of some BAs in psoriasiform dermatitis.

Methods: Pubmed and other public sources were used to survey the literature relevant to the topic of bile acids and their potential use in psoriasis.

Conclusion: There is clinical and preclinical evidence to support a potential role for BA Supplementation (or modulation BA metabolism and signaling) in the treatment of psoriasis.

Keywords: bile acids; dermatitis; inflammation; psoriasis.

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Conflict of interest statement

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Bile Acid Synthesis and Enterohepatic Recycling. Primary bile acids are synthesized in the liver and stored in the gallbladder. In response to food intake, they are released into the duodenum to assist with lipid digestion and emulsification. Most bile acids are reabsorbed in the terminal ileum and return to the liver via enterohepatic recycling. A subset enters the colon and are further metabolized by the gut microbiota.
Figure 2.
Figure 2.
Proposed Mechanisms for Bile Acid Inhibition of IL-17a Production. Secondary bile acids inhibit the production of IL-17a. Potential mechanisms of action underlying this blockade include (A) downregulation of Rorc gene expression or (B) physical binding and obstruction of the activity of the RORγt transcription factor.

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