ArticleThe Journal of investigative dermatology2014
The pattern recognition receptor NOD2 mediates Staphylococcus aureus-induced IL-17C expression in keratinocytes.
Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 83 citations in OpenAlex.
- Hidradenitis suppurativa: epidemiology, diagnosis, molecular pathogenesis and therapy.Molecular biomedicine · 2026Review
- PPARα deficiency causes skin dysbiosis and triggers innate immunity in keratinocytes.Cell death & disease · 2026Article
- Targeting NLRP10 in Atopic Dermatitis: An Emerging Strategy to Modulate Epidermal Cell Death and Barrier Function.International journal of molecular sciences · 2025Review
- Atopic dermatitis-related anti-inflammatory in vitro effects of a plant extract mixture.Scientific reports · 2025Article
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- IL-17C is a driver of damaging inflammation during Neisseria gonorrhoeae infection of human Fallopian tube.Nature communications · 2024Article
- Genetic and Immunological Pathogenesis of Atopic Dermatitis.The Journal of investigative dermatology · 2024Review
- Suppression of TCF4 promotes a ZC3H12A-mediated self-sustaining inflammatory feedback cycle involving IL-17RA/IL-17RE epidermal signaling.JCI insight · 2024Article
- IL-17 Inhibition: A Valid Therapeutic Strategy in the Management of Hidradenitis Suppurativa.Pharmaceutics · 2023Review
- Staphylococcus Aureus and Streptococcus Pyogenes Induce Psoriasis-Related Transcriptomes Augmented by IL-17A and TNF-α.The Journal of investigative dermatology · 2023Article
- NOD2 Agonism Counter-Regulates Human Type 2 T Cell Functions in Peripheral Blood Mononuclear Cell Cultures: Implications for Atopic Dermatitis.Biomolecules · 2023Article
- Skin Care Product Rich in Antioxidants and Anti-Inflammatory Natural Compounds Reduces Itching and Inflammation in the Skin of Atopic Dermatitis Patients.Antioxidants (Basel, Switzerland) · 2022Article
- Platelet-Released Growth Factors Influence Wound Healing-Associated Genes in Human Keratinocytes and Ex Vivo Skin Explants.International journal of molecular sciences · 2022Article
- Staphylococcus aureus Activates the Aryl Hydrocarbon Receptor in Human Keratinocytes.Journal of innate immunity · 2022Article
- Inflammatory Response AgainstFrontiers in immunology · 2022Article
- Platelet-Released Growth Factors Induce Genes Involved in Extracellular Matrix Formation in Human Fibroblasts.International journal of molecular sciences · 2021Article
- Effect of 1-MHz ultrasound on the proinflammatory interleukin-6 secretion in human keratinocytes.Scientific reports · 2021Article
- IL-17C and IL-17RE Promote Wound Closure in aMicroorganisms · 2021Article
- Inborn Errors in the LRR Domain of Nod2 and Their Potential Consequences on the Function of the Receptor.Cells · 2021Review
- IL-6 effector function of group 2 innate lymphoid cells (ILC2) is NOD2 dependent.Science immunology · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-17C is an important epithelial cell-derived cytokine activating innate immunity by the induction of antimicrobial peptides and cytokines. Here, we investigated the role of the cytosolic pattern recognition receptor nucleotide-binding oligomerization domain-containing protein 2 (NOD2) for the Staphylococcus aureus-mediated induction of IL-17C. Activation of NOD2 in HEK293 cells overexpressing NOD2 induced the IL-17C promoter, an activity that was significantly reduced in cells overexpressing the Crohn's disease-associated NOD2 mutation 3020insC (1007fs) or the Crohn's disease- and atopic dermatitis-associated NOD2-R702W variant. The first NF-κB-binding site in the IL-17C promoter was critical for NOD2-mediated IL-17C induction. Infection of human primary keratinocytes with S. aureus induced NOD2 and IL-17C gene expression. Overexpression of NOD2 in keratinocytes augmented S. aureus-mediated IL-17C gene expression as compared with NOD2-R702W overexpression. S. aureus-induced IL-17C expression was diminished in NOD2 small interfering RNA (siRNA)-treated keratinocytes. Moreover, significantly less S. aureus bacteria survived in keratinocytes overexpressing NOD2 but not in cells overexpressing the NOD2-R702W variant. Finally, S. aureus showed an increased survival in keratinocytes treated with NOD2 or IL-17C siRNA. In summary, our study provides evidence that S. aureus activates NOD2 in keratinocytes, resulting in an increased expression of IL-17C, a mechanism that may be dysregulated in atopic dermatitis.
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