The following is a summary of “Rapid reduction in Staphylococcus aureus in atopic dermatitis subjects following dupilumab treatment,” published in the NOVEMBER 2023 issue of Allergy & Immunology by Simpson, et al.

For a study, researchers sought to characterize changes in the host-microbial interface in individuals with atopic dermatitis (AD) following type 2 blockade with dupilumab. The focus was on assessing the impact of dupilumab on Staphylococcus aureus colonization and its correlation with clinical outcomes and immune responses.

Seventy-one participants with moderate-severe AD underwent a randomized, double-blind trial comparing dupilumab to placebo (2:1 ratio). Various assessments were conducted at multiple time points, including quantification of S. aureus and its virulence factors, 16s ribosomal RNA microbiome analysis, serum biomarker measurements, skin transcriptomic analyses, and peripheral blood T-cell phenotyping.

At baseline, all participants exhibited S. aureus colonization on the skin surface. Dupilumab treatment resulted in a rapid and significant reduction in S. aureus levels after only three days, preceding clinical improvement by 11 days. Participants with the most substantial reductions in S. aureus displayed the best clinical outcomes, and these reductions correlated with decreases in serum CCL17 levels and AD severity. Additionally, reductions in S. aureus cytotoxins, alterations in T_H17-cell subsets, and increased expression of genes related to IL-17, neutrophils, and complement pathways were observed.

Blocking IL-4 and IL-13 signaling with dupilumab swiftly reduced S. aureus abundance in individuals with AD. The reduction correlated with improvements in type 2 biomarkers, disease severity, and clinical outcomes. Immunoprofiling and transcriptomic analyses suggested potential involvement of T<sub style=”vertical-align: sub;”>H</sub>17 cells, neutrophils, and complement activation as mechanisms underlying these therapeutic effects.

Source: jacionline.org/article/S0091-6749(23)00754-6/fulltext