ArticleMucosal immunology2018
C3a receptor antagonism as a novel therapeutic target for chronic rhinosinusitis.
Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 24 citations in OpenAlex.
- CD25 expression marks an activated mast cell population in human nasal polyposis.The Journal of allergy and clinical immunology · 2026Article
- Use of Machine Learning and 71-Plex Immune Mediator Analysis to Identify Nasal Mucus Biomarkers Associated With Olfactory Loss in Patients with CRSwNP.American journal of rhinology & allergy · 2026Article
- Chronic Rhinosinusitis with Nasal Polyps: A "Module-First" Review of Murine Models and Chemical Interventions.Molecules (Basel, Switzerland) · 2026Review
- What can we learn about chronic rhinosinusitis through mucus?Current opinion in otolaryngology & head and neck surgery · 2026Review
- Animal models of fungus-related allergic airway disease: exposures, readouts, mechanisms, and translational gaps.Frontiers in cellular and infection microbiology · 2026Review
- Emerging roles for complement in lung transplantation.The Journal of clinical investigation · 2025Review
- Intranasal Calcitriol Accelerates Improvement of Sinonasal Inflammation and Olfactory Impairment in Mice After Cessation of Chronic Cigarette-Smoke Exposure.International forum of allergy & rhinology · 2025Article
- Complement's involvement in allergic Th2 immunity: a cross-barrier perspective.The Journal of clinical investigation · 2025Review
- Exploring the comorbidity association and biological mechanisms of chronic rhinosinusitis and chronic obstructive pulmonary disease.Scientific reports · 2025Article
- Local complement activation and modulation in mucosal immunity.Mucosal immunology · 2024Review
- Review
- MEX3B inhibits collagen production in eosinophilic nasal polyps by downregulating epithelial cell TGFBR3 mRNA stability.JCI insight · 2023Article
- Analysis of competing endogenous RNA (ceRNA) crosstalk in eosinophilic chronic rhinosinusitis with nasal polyps.International forum of allergy & rhinology · 2022Article
- Utilization of Nasal Mucus to Investigate the Pathophysiology of Chronic Rhinosinusitis.American journal of rhinology & allergy · 2022Review
- Role of C3a as a Novel Regulator of 25(OH)DJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Current Insights on the Impact of Proteomics in Respiratory Allergies.International journal of molecular sciences · 2022Review
- Time-dependent effect of desensitization with wasp venom on selected parameters of the immune system.Scientific reports · 2022Article
- M2 macrophage-related gene signature in chronic rhinosinusitis with nasal polyps.Frontiers in immunology · 2022Article
- Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces.European journal of immunology · 2020Review
- Linking Complement C3 and B Cells in Nasal Polyposis.Journal of immunology research · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic rhinosinusitis with nasal polyps (CRSwNP) is an inflammatory disease with an unknown etiology. Recent studies have implicated the complement system as a potential modulator of disease immunopathology. We performed proteomic pathway enrichment analysis of differentially increased proteins, and found an enrichment of complement cascade pathways in the nasal mucus of individuals with CRSwNP as compared to control subjects. Sinonasal mucus levels of complement 3 (C3) correlated with worse subjective disease severity, whereas no significant difference in systemic C3 levels could be determined in plasma samples. Given that human sinonasal epithelial cells were the predominate sinonasal source of C3 and complement anaphylatoxin 3a (C3a) staining, we focused on their role in in vitro studies. Baseline intracellular C3 levels were higher in CRSwNP cells, and following exposure to Aspergillus fumigatus (Af) extract, they released significantly more C3 and C3a. Inhibition of complement 3a receptor (C3aR) signaling led to a decrease in Af-induced C3 and C3a release, both in vitro and in vivo. Finally, we found in vivo that C3aR deficiency or inhibition significantly reduced inflammation and CRS development in a mouse model of Af-induced CRS. These findings demonstrate that local sinonasal complement activation correlates with subjective disease severity, and that local C3aR antagonism significantly ameliorates Af-induced CRS in a rodent model.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.