ArticleMucosal immunology2019
FcγRIII stimulation breaks the tolerance of human nasal epithelial cells to bacteria through cross-talk with TLR4.
Article in Mucosal immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
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- Multi-scale transcriptomic integration reveals epithelial state heterogeneity and remodeling-associated transcriptomic clusters in chronic rhinosinusitis with nasal polyps.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026Article
- Development of in vitro airway epithelial model to assess immune response and safety of mucosal adjuvants.NPJ vaccines · 2026Article
- Internalization and Colocalization of a Polyclonal Antibody Against Porphyromonas gingivalis FimA type I in Infected Cells.European journal of dentistry · 2025Article
- Differential Immune Cell Infiltration in Eosinophilic and Non-Eosinophilic CRS: Correlations With Clinical, Endoscopic, and Radiological Findings.International forum of allergy & rhinology · 2025Article
- Intracellular bacterial LPS drives pyroptosis and promotes aggressive phenotype in oral squamous cell carcinoma.Medical oncology (Northwood, London, England) · 2025Article
- A user's guide to designing efficient and safe mucosal vaccines: Challenges & potentials.Oxford open immunology · 2025Review
- Analysis of BeyfortusCurrent issues in molecular biology · 2024Review
- Epithelial innate immune response to Pseudomonas aeruginosa-derived flagellin in chronic rhinosinusitis.International forum of allergy & rhinology · 2023Article
- Role of FcγRIII in the nasal cavity of BALB/c mice in the primary amebic meningoencephalitis protection model.Parasitology research · 2023Article
- Review
- Leveraging Antibody, B Cell and Fc Receptor Interactions to Understand Heterogeneous Immune Responses in Tuberculosis.Frontiers in immunology · 2022Review
- The Role of IgA in Chronic Upper Airway Disease: Friend or Foe?Frontiers in allergy · 2022Review
- M2 macrophage-related gene signature in chronic rhinosinusitis with nasal polyps.Frontiers in immunology · 2022Article
- High titers and low fucosylation of early human anti-SARS-CoV-2 IgG promote inflammation by alveolar macrophages.Science translational medicine · 2021Article
- Review
- mTOR-driven glycolysis governs induction of innate immune responses by bronchial epithelial cells exposed to the bacterial component flagellin.Mucosal immunology · 2021Article
- The Importance of Glycosylation in COVID-19 Infection.Advances in experimental medicine and biology · 2021Article
- Novel Antioxidant Therapy with the Immediate Precursor to Glutathione, γ-Glutamylcysteine (GGC), Ameliorates LPS-Induced Cellular Stress in In Vitro 3D-Differentiated Airway Model from Primary Cystic Fibrosis Human Bronchial Cells.Antioxidants (Basel, Switzerland) · 2020Article
- Impact of Glycosylation and Species Origin on the Uptake and Permeation of IgGs through the Nasal Airway Mucosa.Pharmaceutics · 2020Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nasal cavity displays immune tolerance to commensal bacteria under homeostatic conditions, which is rapidly converted to a pro-inflammatory response upon infection. Yet, the factors that control this conversion are still largely unknown. Here, we provide evidence that Fc gamma receptor III (FcγRIII) stimulation breaks immune tolerance to bacteria in the human nasal cavity through activation of nasal epithelial cells, which are the first line of defense against invading microbes. While under steady-state conditions human nasal epithelial cells were completely non-responsive to Gram-negative bacteria P. aeruginosa or TLR4 ligand LPS, IgG opsonization of bacteria, as occurs upon infection, strongly induced production of pro-inflammatory agents such as IL-6 and IL-8. This breaking of tolerance to bacteria was completely dependent on FcγRIII, which amplified cytokine gene transcription through cross-talk with TLR4. In addition, we identified that epithelial cells from patients suffering from chronic rhinosinusitis with nasal polyps do not display LPS tolerance, thereby providing an explanation for the disturbed host defense responses of these patients. Taken together, these data are the first to identify FcγR expression on nasal epithelial cells, as well as to identify its important role in controlling the balance between tolerance and inflammation in the nasal cavity.
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