Head and neck dermatitis is exacerbated by colonization, skin barrier disruption, and immune dysregulation.

Introduction & Objectives: Head and neck dermatitis (HND) is a refractory phenotype of atopic dermatitis (AD) and can be a therapeutic challenge due to lack of responsiveness to conventional treatments. Previous studies have suggested that the microbiome and fungiome may play a role in inducing HND, but the underlying pathogenic mechanisms remain unknown. This study aimed to determine the link between HND and fungiome and to examine the contribution of .

Materials And Methods: To identify the effect of the sensitization status of on HND, 312 patients diagnosed with AD were enrolled. To elucidate the mechanism underlying the effects of , human keratinocytes and dermal endothelial cells were cultured with and treated with Th2 cytokines. The downstream effects of various cytokines, including inflammation and angiogenesis, were investigated by real-time quantitative PCR. To identify the association between changes in lipid composition and sensitization status, D-squame tape stripping was performed. Lipid composition was evaluated by focusing on ceramide species using liquid chromatography coupled with tandem mass spectrometry.

Results: Increased sensitization to was observed in patients with HND. Additionally, sensitization to was associated with increased disease severity in these patients. IL-4 treated human keratinocytes cultured with produced significantly more VEGF, VEGFR, IL-31, and IL-33. IL-4/ co-cultured dermal endothelial cells exhibited significantly elevated VEGFR, TGF-β, TNF-α, and IL-1β levels. Stratum corneum lipid analysis revealed decreased levels of esterified omega-hydroxyacyl-sphingosine, indicating skin barrier dysfunction in HND. Finally, growth was inhibited by the addition of these ceramides to culture media, while the growth of other microbiota, including , were not inhibited.

Conclusions: Under decreased levels of ceramide in AD patients with HND, would proliferate, which may enhance pro-inflammatory cytokine levels, angiogenesis, and tissue remodeling. Thus, it plays a central role in the pathogenesis of HND in AD.