Thin-film electronic devices can be integrated with skin for health monitoring and/or for interfacing with machines. Minimal invasiveness is highly desirable when applying wearable electronics directly onto human skin. However, manufacturing such on-skin electronics on planar substrates results in limited gas permeability. Therefore, it is necessary to systematically investigate their long-term physiological and psychological effects. As a demonstration of substrate-free electronics, here we show the successful fabrication of inflammation-free, highly gas-permeable, ultrathin, lightweight and stretchable sensors that can be directly laminated onto human skin for long periods of time, realized with a conductive nanomesh structure. A one-week skin patch test revealed that the risk of inflammation caused by on-skin sensors can be significantly suppressed by using the nanomesh sensors. Furthermore, a wireless system that can detect touch, temperature and pressure is successfully demonstrated using a nanomesh with excellent mechanical durability. In addition, electromyogram recordings were successfully taken with minimal discomfort to the user.
Loss-of-function mutations in the filaggrin gene (FLG), cause the semi-dominant keratinizing disorder, ichthyosis vulgaris1, and convey major genetic risk to atopic dermatitis/eczema, eczema-associated asthma2,3 and other allergic phenotypes5. Several low frequency FLG null alleles occur in Europeans and Asians, with a cumulative frequency of ~9% in Europe4. Here we report a 1-bp deletion mutation, 5303delA, highly analogous to common human FLG mutations, within the murine flg gene in the spontaneous mouse mutant flaky tail (ft). Importantly, we demonstrate that topical application of allergen to mice homozygous for this mutation results in cutaneous inflammatory infiltrates and enhanced cutaneous allergen priming with development of allergen-specific antibody responses. These data validate ft as a useful model of filaggrin deficiency and provide experimental evidence for the hypothesis that antigen transfer through a defective epidermal barrier is a key mechanism underlying elevated IgE sensitization and initiation of cutaneous inflammation in humans with filaggrin-related atopic disease.
Summary
Staphylococcus aureus skin colonization is universal in atopic
dermatitis and common in cancer patients treated with epidermal growth factor receptor
inhibitors. However, the causal relationship of dysbiosis and eczema has yet to be
clarified. Herein, we demonstrate that
Adam17fl/flSox9-Cre mice,
generated to model ADAM17-deficiency in human, developed eczematous
dermatitis with naturally occurring dysbiosis, similar to that observed in atopic
dermatitis. Corynebacterium mastitidis, S. aureus, and
Corynebacterium bovis sequentially emerged during the onset of
eczematous dermatitis, and antibiotic specific for these bacterial species almost
completely reversed dysbiosis and eliminated skin inflammation. Whereas S.
aureus prominently drove eczema formation, C. bovis induced
robust T helper 2 cell responses. Langerhans cells were required for eliciting immune
responses against S. aureus inoculation. These results characterize
differential contributions of dysbiotic flora during eczema formation, and highlight the
microbiota-host immunity axis as a possible target for future therapeutics in eczematous
dermatitis.
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