Introduction:

Staphylococcus aureus typically colonizes the anterior nares of 20-30% of healthy individuals, with transient colonization occurring on the skin. Notably, the situation is markedly different in patients with atopic dermatitis (AD). Here, S. aureus is frequently isolated from skin samples, and its prevalence increases with disease severity. The regulatory processes that facilitate the transition from an asymptomatic nasal colonizer to a pathogen associated with symptomatic skin disease remain unknown.

Methods:

To gain insight into the regulatory adaption mechanisms that promote the transition from a commensal to a pathogen associated with symptomatic skin diseases, we analyzed the in vivo transcriptional profile of S. aureus colonizing the nose and non-diseased skin, as opposed to diseased skin of patients with AD, by quantitative real-time PCR.

Results:

The transcriptional profile during asymptomatic colonization of the nose or non-lesional skin closely resembled that of lesional skin samples for many of the genes studied with elevated expression of genes that encode adhesion-related proteins and proteases. In addition, genes that modify and maintain the cell wall and encode proteins that facilitate immune evasion showed increased transcriptional activity during both colonization and infection. Notably, in a subgroup of patients, the peptide quorum sensing system Agr (accessory gene regulator) and downstream target genes were inactive during nasal colonization but upregulated in lesional and non-lesional skin samples.

Conclusions:

Taken together, our results demonstrate an infection-like transcriptional profile during colonization and suggest a role for the Agr system during the transition from asymptomatic colonization to infection.