Staphylococcus aureus and Atopic Dermatitis: A Complex and Evolving Association

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with pruritus and epidermal barrier dysfunction. A key contributor to AD pathogenesis is Staphylococcus aureus (S. aureus), which colonizes the skin of affected individuals, exacerbating disease severity through toxin production and immune dysregulation. The microbiota of AD patients is significantly altered, with a reduction in microbial diversity and antimicrobial peptides, leading to an imbalance favoring S. aureus. The bacterium disrupts epidermal integrity, induces inflammasome activation, and promotes apoptosis, further worsening the inflammatory response. Methicillin-resistant S. aureus (MRSA) colonization poses a significant challenge in managing AD due to antibiotic resistance.

Multiple factors contribute to S. aureus dominance in AD skin, including genetic predisposition, altered immune responses, and environmental triggers. Th2/Th17 cytokine profiles are elevated in AD patients, leading to increased susceptibility to microbial invasion and inflammation. Filaggrin mutations, a common genetic trait in AD, further compromise the skin barrier, facilitating bacterial colonization. Treatment strategies include topical and systemic antibiotics, monoclonal antibodies, microbiome transplantation, and bacteriophage therapy. However, antibiotic resistance necessitates novel therapeutic approaches, such as targeting virulence factors, modulating immune responses, and restoring microbiome balance.

Recent studies emphasize the role of commensal Staphylococcus species in protecting against S. aureus colonization, highlighting the potential of microbiome-based interventions. Future research should focus on developing targeted therapies that restore skin homeostasis while minimizing antibiotic resistance. Understanding the intricate relationship between S. aureus and AD will aid in refining treatment strategies and improving patient outcomes.