Neutralizing Interleukin-13 with Tralokinumab Reduces Abundance of S. aureus in Adolescents with Atopic Dermatitis

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Lisa Beck
Stephan Weidinger
Marie Tauber
Hidehisa Saeki
Alan Irvine
Lawrence Eichenfield
Thomas Werfel
Petra Arlert
Azra Kurbasic
Mads Røpke
Amy Paller

Keywords

atopic dermatitis, tralokinumab

Abstract

Patients with atopic dermatitis (AD) are frequently colonized with high levels of S. aureus. Dysregulation of the skin microbiome in AD is influenced by epidermal barrier disruption and type 2 inflammation. Tralokinumab is a high-affinity, monoclonal antibody that targets IL-13, a key driver of type 2 inflammation. We assessed S. aureus abundance in lesional and non-lesional skin and evaluated the effects of tralokinumab on S. aureus abundance in adolescents with moderate-to-severe AD (ECZTRA 6, NCT03526861). 301 adolescents (aged 12-17 years) were randomized to receive tralokinumab 150mg or 300mg SQ every 2 weeks, or placebo. Skin swabs collected from lesional and non-lesional skin at baseline and Week 16 were assessed for S. aureus abundance by femA qPCR. Differences in percentage of S. aureus+ (SA+; defined as >1.07 gene copies/cm2) patients among the groups were assessed using a logistic regression model adjusting for baseline SA status and rescue use (any TCI, TCS, or systemic treatment). From baseline to Week 16, the percentage of patients with SA+ lesional skin was reduced from 83.5% to 41.0% with tralokinumab 150 mg and from 84.3% to 41.9% with tralokinumab 300 mg compared to 85.2% to 78.3% with placebo (difference vs placebo 150mg/300mg: -41.0/-39.6; P<0.001). The percentage of patients with SA+ non-lesional skin was reduced from 78.7% to 34.6% with tralokinumab 150 mg and from 72.2% to 42.4% with tralokinumab 300 mg compared to 74.4% to 68.8% with placebo (difference vs placebo 150mg/300mg: -37.0/-26.1; P≤0.001) from baseline to Week 16. These data support the targeting of IL-13 in improving AD-associated dysbiosis in adolescents.

References

1. Edslev S, et al. Acta Derm Venereol. 2020; 100(12):adv00164.

2. Biedermann T, et al. Front Immunol. 2015;6:353.

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