# Microbiome dysbiosis and therapeutic restoration in atopic dermatitis

## TL;DR

This paper reviews how skin microbiome imbalances contribute to atopic dermatitis and explores new treatments targeting these imbalances.

## Contribution

The paper introduces the potential of microbiome-targeted therapies, including bacteriotherapy and phage therapy, for treating atopic dermatitis.

## Key findings

- Microbiome dysbiosis in AD is marked by overgrowth of Staphylococcus aureus and Malassezia species.
- Host factors like reduced antimicrobial peptides and elevated skin pH promote S. aureus colonization.
- Precision phage therapy and commensal bacteria show promise for restoring skin microbiome balance.

## Abstract

Atopic dermatitis (AD) is increasingly recognized as a chronic inflammatory skin disease driven by a self-reinforcing vicious cycle involving skin barrier dysfunction, immune dysregulation, and cutaneous microbiome dysbiosis. A hallmark of this dysbiosis is the overrepresentation of pathogens like Staphylococcus aureus and Malassezia species, alongside a marked loss of microbial diversity, particularly during disease flares. This review systematically dissects the host-derived factors—such as altered lipid profiles, reduced antimicrobial peptides, and elevated skin pH—that facilitate S. aureus colonization. We further examine how bacterial virulence factors amplify type 2 inflammation and impair barrier integrity, thereby sustaining the pathological loop. We also explore the emerging roles of the skin virome, particularly the phageome, and discuss how microbiome-targeted interventions, including bacteriotherapy with commensal bacteria and precision phage therapy, offer promising avenues for ecological restoration. Finally, we argue that future research must leverage multi-omics to understand strain-specific functions, ultimately guiding the development of personalized microbiome interventions for AD.