# Therapeutic Mechanism of Kynurenine, a Metabolite of Probiotics, on Atopic Dermatitis in Mice

## TL;DR

This study shows that kynurenine, a metabolite from probiotics, can reduce atopic dermatitis symptoms in mice by improving gut health and immune responses.

## Contribution

The novel finding is that kynurenine from specific probiotics alleviates AD through the gut–skin axis by modulating immune markers and intestinal barrier function.

## Key findings

- Kynurenine supplementation reduces AD symptoms in mice by lowering IgE, IL-4, IL-5, IL-13, and TSLP levels.
- Kynurenine improves intestinal short-chain fatty acid levels and repairs intestinal barrier function in AD mice.
- The therapeutic effects of kynurenine are linked to the gut–skin axis and immune modulation.

## Abstract

Atopic Dermatitis (AD) is a common inflammatory skin disease characterized primarily by its chronic and recurrent nature. This has a significant impact on productivity and human longevity. Dysbiosis of gut flora has been demonstrated to be significantly associated with the progression of AD. In our previous research, it was shown that Lactobacillus rhamnosus RL5-H3-005 (RL) and Pediococcus acidilactici RP-H3-006 (RP) have the ability to reduce the risk of disease in AD mice through the gut–mammary axis. Based on our previous work, this study aims to further investigate the effects of kynurenine (KYN), a metabolite of RL and RP, on AD mice induced by 2, 4-dinitrofluorobenzene (DNFB). In this study, we found that supplementing KYN in AD mice effectively alleviates the pathological symptoms of atopic dermatitis and further improves the levels of SCFAs in their intestines. Further research indicates that KYN’s therapeutic effects on AD are primarily manifested in the reduction of secretory immunoglobulin A (sIgA), immunoglobulin E (IgE), interleukin-4 (IL-4), IL-5, IL-13, and thymic stromal lymphopoietin (TSLP) levels in mice, while also repairing the intestinal barrier function of AD mice. Overall, the metabolites KYN of probiotics RL and RP can regulate the levels of SCFAs of mice, potentially improving the symptoms of AD mice through the gut–skin axis.