In atopic dermatitis, skin dryness and recurrent eczema are associated. In patients with Alzheimer's disease, the risk of developing a Staphylococcus aureus skin infection is increased. In this study, researchers investigated how S. aureus infection could modulate and exacerbate skin dryness, through a type 2 inflammatory mechanism. In vivo, infection triggered the release of IL-33, induced by skin delipidation, exacerbating cutaneous inflammation. In mouse models, the researchers were able to attenuate IL-33 release from S. aureus-infected keratinocytes. This release is thought to be associated with necroptosis-type cell death pathways.
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