Temporal relationships between Staphylococcus aureus colonization, filaggrin expression, and pediatric atopic...

Area of Science:

• Dermatology
• Microbiology
• Pediatrics

Background:

• Atopic dermatitis (AD) is frequently associated with Staphylococcus aureus (S. aureus) colonization.
• Limited longitudinal data exists on the interplay between early-life S. aureus colonization, skin barrier function, and AD development.
• Understanding these relationships is crucial for defining early-life AD pathogenesis.

Purpose of the Study:

• To define longitudinal S. aureus skin colonization endotypes in early life.
• To investigate the association between S. aureus colonization phenotypes and AD severity, sensitization, and skin barrier function.
• To explore the relationship between S. aureus colonization and filaggrin (FLG) expression over time.

Main Methods:

• Defined longitudinal S. aureus colonization phenotypes (non-colonized, early transient, late-onset, persistent) over two annual visits in the 'Mechanisms of Progression of Atopic Dermatitis to Asthma in Children' cohort.
• Analyzed AD severity (SCORAD), sensitization, and skin barrier function (FLG expression) across these phenotypes.
• Conducted mediation analyses to assess the relationship between colonization and FLG expression.

Main Results:

• Persistent S. aureus colonization was significantly associated with increased AD severity (SCORAD) and decreased non-lesional (NL) FLG expression at both visits compared to non-colonized individuals.
• Children colonized at the second visit showed a significant decrease in NL-FLG expression from the first to the second visit compared to those who remained non-colonized.
• This decrease in FLG expression remained significant even after adjusting for baseline colonization and AD severity.

Conclusions:

• This study provides the first longitudinal data on FLG expression and S. aureus colonization in early life.
• Findings suggest that a decline in NL-FLG expression may precede and drive S. aureus colonization.
• Therapies aimed at maintaining NL-FLG expression could potentially prevent S. aureus colonization and impact AD progression, highlighting persistent colonization as a longitudinal AD endotype characterized by increased severity and decreasing FLG.