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

Abstract

Atopic dermatitis (AD) is characterized by cutaneous dysbiosis marked by Staphylococcus aureus overgrowth, reduced commensal diversity, barrier dysfunction, and chronic inflammation. We investigated acacia gum (AG) as a topical prebiotic to modulate staphylococcal community structure and biofilm ecology in AD. Using both in vitro and in vivo approaches, we examined how AG reshaped microbial interactions and host responses. In coculture systems, AG selectively promoted Staphylococcus epidermidis while suppressing S. aureus. The S. aureus growth inhibition by AG involved direct antibacterial activity and commensal-mediated effects. We found that AG-upregulated glutamyl endopeptidase in S. epidermidis played a role in suppressing S. aureus colonization. AG disrupted both developing and established S. aureus biofilms and reduced intracellular persistence within macrophages, indicating activity across extracellular and host-associated niches. Beyond microbiota modulation, AG attenuated keratinocyte and macrophage activation via downregulation of proinflammatory cytokines and chemokines. In an AD-like mouse model, topical AG reduced S. aureus burden by three orders of magnitude, improved microbial diversity, partially restored barrier integrity, and decreased inflammatory cell infiltration without detectable toxicity. Collectively, AG reprograms staphylococcal dysbiosis and biofilm stability, supporting microbiota-directed prebiotic modulation as a mechanistically defined strategy for AD.