ArticleScientific reports2016
Natural killer cells regulate eosinophilic inflammation in chronic rhinosinusitis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Natural Killer Cell Dysfunction Causes Eosinophil Accumulation in Chronic Rhinosinusitis With Nasal Polyps.Clinical and translational allergy · 2026Article
- TLR7 Promotes Acute Inflammatory-Driven Lung Dysfunction in Influenza-Infected Mice but Prevents Late Airway Hyperresponsiveness.International journal of molecular sciences · 2024Article
- Chronic stimulation desensitizes β2-adrenergic receptor responses in natural killer cells.European journal of immunology · 2024Article
- Sweet taste receptor agonists attenuate macrophage IL-1β expression and eosinophilic inflammation linked to autophagy deficiency in myeloid cells.Clinical and translational medicine · 2022Article
- Chronic Rhinosinusitis,Biomedicines · 2022Review
- Ginsenoside F1 Attenuates Eosinophilic Inflammation in Chronic Rhinosinusitis by Promoting NK Cell Function.Journal of ginseng research · 2021Article
- Comparison of Blood and Tissue Eosinophil Count and Blood IgE in Patients with Chronic Sinusitis and Nasal Polyps.Journal of immunology research · 2021Article
- Immune cell infiltration and related core genes expression characteristics in eosinophilic and non-eosinophilic chronic rhinosinusitis with nasal polyps.Experimental and therapeutic medicine · 2020Article
- Assessment of NK Cell Activity Based on NK Cell-Specific Receptor Synergy in Peripheral Blood Mononuclear Cells and Whole Blood.International journal of molecular sciences · 2020Article
- The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy.International journal of molecular sciences · 2020Review
- CXCR5-negative natural killer cells ameliorate experimental autoimmune myasthenia gravis by suppressing follicular helper T cells.Journal of neuroinflammation · 2019Article
- Role of Natural Killer Cells in Airway Inflammation.Allergy, asthma & immunology research · 2018Review
- Enhanced Interferon-β Response Contributes to Eosinophilic Chronic Rhinosinusitis.Frontiers in immunology · 2018Article
- Sinonasal T-cell expression of cytotoxic mediators granzyme B and perforin is reduced in patients with chronic rhinosinusitis.American journal of rhinology & allergy · 2017Article
- Protective Roles for RGS2 in a Mouse Model of House Dust Mite-Induced Airway Inflammation.PloS one · 2017Article
- Sinus Surgery Is Associated with a Decrease in Aspirin-Induced Reaction Severity in Patients with Aspirin Exacerbated Respiratory Disease.The journal of allergy and clinical immunology. In practiceObservational
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eosinophils play a major pathologic role in the pathogenesis of diverse inflammatory diseases including chronic rhinosinusitis (CRS). Dysregulated production of prostaglandin (PG), particularly PGD2, is considered to be an important contributing factor to eosinophilic inflammation in CRS primarily through proinflammatory and chemotactic effects on eosinophils. Here, we provide evidence that PGD2 can promote eosinophilic inflammation through a suppression of Natural killer (NK) cell effector function and NK cell-mediated eosinophil regulation. Eosinophil apoptosis mediated by NK cells was significantly decreased in CRS patients compared with healthy controls. This decrease was associated with NK cell dysfunction and eosinophilic inflammation. Tissue eosinophils were positively correlated with blood eosinophils in CRS patients. In a murine model of CRS, NK cell depletion caused an exacerbation of blood eosinophilia and eosinophilic inflammation in the sinonasal tissue. PGD2 and its metabolite, but not PGE2 and a panel of cytokines including TGF-β, were increased in CRS patients compared with controls. Effector functions of NK cells were potently suppressed by PGD2-dependent, rather than PGE2-dependent, pathway in controls and CRS patients. Thus, our results suggest decreased NK cell-mediated eosinophil regulation, possibly through an increased level of PGD2, as a previously unrecognized link between PG dysregulation and eosinophilic inflammation in CRS.
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