ArticleCell reports2025
Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Fibroblasts resistScience advances · 2026Article
- Update on environmental determinants of allergic diseases.The Journal of allergy and clinical immunology · 2026Review
- Atopic march protocol involving sequential skin and lung inflammation elicited by epicutaneous Staphylococcus aureus and allergen exposure.STAR protocols · 2026Article
- Evidence for murine cutaneous immune surveillance localized to hair follicle epithelium.Frontiers in cell and developmental biology · 2026Article
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Authors and funding
14 authors.
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Abstract
Patients with atopic dermatitis exhibit abundant Staphylococcus aureus skin colonization and an increased risk of atopic march diseases, including allergic rhinitis, food allergies, and asthma. We have previously shown that S. aureus skin exposure exacerbates allergic lung inflammation in an interleukin-36 receptor (IL-36R)-dependent manner. However, the cellular and molecular mechanisms by which S. aureus skin exposure and IL-36R signaling orchestrate the progression from skin to lung inflammation are unclear. Using a preclinical model of the atopic march, we found that S. aureus skin exposure promoted robust neutrophilic lung inflammation via keratinocyte- and lung epithelia-specific IL-36R signaling. Unexpectedly, neutrophil IL-36R signaling triggered neutrophil extracellular trap (NET) formation and augmented lung pathology. Importantly, anti-IL-36R monoclonal antibody (mAb) treatment prevented the development of neutrophilic lung inflammation. Collectively, our findings suggested that S. aureus skin exposure exacerbates lung inflammation via distinct IL-36R signaling mechanisms on epithelia and neutrophils, which has therapeutic potential in halting the progression of the atopic march.
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