ArticleCellular & molecular immunology2016
NOD2 and TLR2 ligands trigger the activation of basophils and eosinophils by interacting with dermal fibroblasts in atopic dermatitis-like skin inflammation.
Article in Cellular & molecular immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- The influence of single nucleotide polymorphisms of NOD2 or CD14 on the risk of Mycobacterium tuberculosis diseases: a systematic review.Systematic reviews · 2021Pooled it
- Recent advances in immunocompetent human skin-on-chip models: Construction strategies and biomedical applications.Bioactive materials · 2026Review
- Integrative Omics of Eosinophils in Asthma and COPD: Deciphering Molecular Signatures for Targeted Therapy.Molecular diagnosis & therapy · 2026Review
- Dermal fibroblasts respond to IL-4 and IL-13 and promote T cell recruitment in atopic dermatitis.The Journal of clinical investigation · 2026Article
- Basophils in atopic dermatitis: Immunologic roles and clinical implications.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2026Review
- A basophil-fibroblast pro-inflammatory axis fuels type 2 skin inflammation.Cell reports · 2025Article
- Understanding the Impact of Ostomy Dejecta Constituents on Peristomal Skin Health and Models for Its Characterisation.International wound journal · 2025Review
- Review
- Article
- The Role of Fibroblasts in Atopic Dermatitis: Establishing Proinflammatory Microenvironments and Mediating Cellular Crosstalk.Journal of inflammation research · 2025Review
- The Role of Basophils in Atopic Dermatitis, from Pathogenesis to Therapeutic Perspectives.Journal of asthma and allergy · 2025Review
- Review
- Stromal cells and epigenetics: emerging key players of chronic inflammatory skin diseases.BMB reports · 2024Review
- Fibroblast: A Novel Target for Autoimmune and Inflammatory Skin Diseases Therapeutics.Clinical reviews in allergy & immunology · 2024Review
- Preclinical Models of Atopic Dermatitis Suitable for Mechanistic and Therapeutic Investigations.Journal of inflammation research · 2024Review
- Effect of Proinflammatory S100A9 Protein on Migration and Proliferation of Microglial Cells.Journal of molecular neuroscience : MN · 2023Article
- Risk of Inflammatory Bowel Disease in Patients With Atopic Dermatitis.JAMA dermatology · 2023Article
- NLRP3 Inflammasome as Therapeutic Targets in Inflammatory Diseases.Biomolecules & therapeutics · 2023Review
- Integrating RNA-sequencing and network analysis to explore the mechanism of topical Pien Tze Huang treatment on diabetic wounds.Frontiers in pharmacology · 2023Article
- Network pharmacology and molecular docking-based prediction of active compounds and mechanisms of action of Cnidii Fructus in treating atopic dermatitis.BMC complementary medicine and therapies · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The skin of patients with atopic dermatitis (AD) has a unique predisposition for colonization by Staphylococcus aureus (S. aureus), which contributes to the inflammation and grim prognosis of AD. Although the mechanism underlying the S. aureus-induced exacerbation of AD remains unclear, recent studies have found a pivotal role for pattern recognition receptors in regulating the inflammatory responses in S. aureus infection. In the present study, we used a typical mouse model of AD-like skin inflammation and found that S. aureus-associated nucleotide-binding oligomerization domain-containing protein 2 (NOD2) and toll-like receptor 2 (TLR2) ligands exacerbated AD-like symptoms, which were further deteriorated by the in vivo expansion of basophils and eosinophils. Subsequent histological analyses revealed that dermal fibroblasts were pervasive in the AD-like skin lesions. Co-culture of human dermal fibroblasts with basophils and eosinophils resulted in a vigorous cytokine/chemokine response to the NOD2/TLR2 ligands and the enhanced expression of intercellular adhesion molecule-1 on the dermal fibroblasts. Basophils and eosinophils were primarily responsible for the AD-related cytokine/chemokine expression in the co-cultures. Direct intercellular contact was necessary for the crosstalk between basophils and dermal fibroblasts, while soluble mediators were sufficient to mediate the eosinophil-fibroblast interactions. Moreover, the intracellular p38 mitogen-activated protein kinase, extracellular signal-regulated kinase, and nuclear factor-kappa B signaling pathways were essential for NOD2/TLR2 ligand-mediated activation of basophils, eosinophils, and dermal fibroblasts in AD-related inflammation. This study provides the evidence of NOD2/TLR2-mediated exacerbation of AD through activation of innate immune cells and therefore sheds light on a novel mechanistic pathway by which S. aureus contributes to the pathophysiology of AD.
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