Topical acacia gum reshapes staphylococcal dysbiosis and inflammation in atopic dermatitis.

Summary

Using in vitro systems and an AD-like mouse model, topical acacia gum selectively favored S. epidermidis over S. aureus, disrupted S. aureus biofilms, reduced intracellular persistence, and dampened inflammatory signaling. These effects collectively reduced S. aureus burden by three logs and partially restored barrier function without detectable toxicity, supporting microbiome-directed prebiotic therapy.

Key Findings

• Acacia gum selectively promoted S. epidermidis while suppressing S. aureus in coculture.
• AG disrupted developing and established S. aureus biofilms and reduced intracellular persistence in macrophages.
• Topical AG reduced S. aureus burden by ~3 logs, improved microbial diversity, partially restored barrier integrity, and decreased inflammatory infiltrates in an AD-like mouse model.
• Upregulation of S. epidermidis glutamyl endopeptidase contributed to suppression of S. aureus colonization.
• AG downregulated proinflammatory cytokines/chemokines in keratinocytes and macrophages without detectable toxicity.

Clinical Implications

Although preclinical, the data justify early-phase clinical trials of acacia gum-containing topicals as adjuncts to standard AD care to lower S. aureus colonization, reduce inflammation, and improve barrier function with favorable safety.

Limitations

• Preclinical study without human subjects; translational efficacy and safety require clinical validation.
• Formulation specifics (dose-ranging, vehicle optimization, long-term effects) are not fully explored.

Future Directions

Conduct dose-ranging and vehicle-optimized phase I/II trials in AD, evaluate durability and microbiome dynamics, and compare with standard antimicrobials or emollients.