# From Gut Dysbiosis to Skin Inflammation in Atopic Dermatitis: Probiotics and the Gut–Skin Axis—Clinical Outcomes and Microbiome Implications

**Authors:** Adina Elena Micu, Ioana Adriana Popescu, Ioana Alina Halip, Mădălina Mocanu, Dan Vâță, Andreea Luana Hulubencu, Dragoș Florin Gheucă-Solovăstru, Laura Gheucă-Solovăstru

PMC · DOI: 10.3390/ijms27010365 · International Journal of Molecular Sciences · 2025-12-29

## TL;DR

This review explores how gut dysbiosis contributes to atopic dermatitis and evaluates the potential of probiotics to improve skin inflammation and symptoms.

## Contribution

The paper provides a comprehensive review of recent clinical and mechanistic evidence on probiotics and the gut–skin axis in atopic dermatitis.

## Key findings

- Multistrain probiotics showed modest improvements in AD severity and biomarkers in pediatric RCTs.
- Probiotics may modulate immune pathways like TLR2/4 and promote anti-inflammatory responses.
- Clinical evidence remains limited by inconsistent outcomes and lack of skin microbiome data.

## Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease in which barrier impairment, immune dysregulation, and gut–skin dysbiosis intersect, prompting growing interest in probiotics as microbiota-modulating adjuncts. We conducted a narrative review of peer-reviewed articles indexed in PubMed, Scopus, and Google Scholar, restricted to publications from 1 January 2018 to 31 October 2025 (searches last run in December 2025). Eligible evidence included randomized controlled trials (RCTs), observational studies, and mechanistic or conceptual reviews addressing microbiome alterations and microbiota-modulating interventions in AD. Most pediatric RCTs using multistrain, Lactobacillus-dominant formulations (often combined with Bifidobacterium) reported modest improvements in AD severity and pruritus and in selected barrier- and inflammation-related biomarkers. However, direct cutaneous microbiome “restoration” outcomes were reported in a minority of studies, and most clinical evidence relies on clinical endpoints and gut–skin axis plausibility rather than longitudinal skin microbiome readouts. Single-strain regimens showed inconsistent effects, and evidence in adolescents and adults remained heterogeneous. Mechanistically, probiotics may enhance short-chain fatty acid (SCFA) signaling, dampen toll-like receptor 2/4 (TLR2/4)-nuclear factor kappa B (NF-κB) activation, and promote interleukin-10 (IL-10)- and transforming growth factor-β (TGF-β)-driven tolerance. Probiotics are a biologically plausible adjunct targeting the gut–skin axis in AD and are generally well tolerated; however, heterogeneity across trials, limited follow-up, inconsistent adverse-event reporting, and scarce skin microbiome endpoints preclude firm clinical recommendations.

## Linked entities

- **Proteins:** TLR2 (toll like receptor 2), TLR4 (toll like receptor 4), NFKB1 (nuclear factor kappa B subunit 1), IL10 (interleukin 10), TGFB1 (transforming growth factor beta 1)
- **Diseases:** atopic dermatitis (MONDO:0004980)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}
- **Diseases:** Gut Dysbiosis (MESH:D064806), immune dysregulation (OMIM:614878), pruritus (MESH:D011537), AD (MESH:D003876), Inflammation (MESH:D007249), skin disease (MESH:D012871)
- **Chemicals:** SCFA (MESH:D005232)
- **Species:** Lactobacillus (genus) [taxon 1578], Bifidobacterium (genus) [taxon 1678]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12785343/full.md

## References

59 references — full list in the complete paper: https://tomesphere.com/paper/PMC12785343/full.md

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Source: https://tomesphere.com/paper/PMC12785343