ArticleInfection and immunity2004
Antifungal immune reactivity in nasal polyposis.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
The trial behind it
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Who cites it
11 citing papers in PubMed, 36 citations in OpenAlex.
- Differential expression of innate immunity genes in chronic rhinosinusitis.American journal of rhinology & allergyTrial
- TLR Signals in Epithelial Cells in the Nasal Cavity and Paranasal Sinuses.Frontiers in allergy · 2021Review
- TLR-2 expression and dysregulated human Treg/Th17 phenotype in Aspergillus flavus infected patients of chronic rhinosinusitis with nasal polyposis.Microbial cell factories · 2020Article
- Different activations of toll-like receptors and antimicrobial peptides in chronic rhinosinusitis with or without nasal polyposis.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 · 2016Article
- Damage-associated molecular patterns and their receptors in upper airway pathologies.Cellular and molecular life sciences : CMLS · 2013Review
- Endotypes and phenotypes of chronic rhinosinusitis: a PRACTALL document of the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma & Immunology.The Journal of allergy and clinical immunology · 2013Article
- Alterations in epithelial barrier function and host defense responses in chronic rhinosinusitis.The Journal of allergy and clinical immunology · 2009Review
- Role of neutrophils in preventing and resolving acute fungal sinusitis.Infection and immunity · 2007Article
- Up-regulation of Toll-like receptors 2, 3 and 4 in allergic rhinitis.Respiratory research · 2005Article
- Perspectives on the etiology of chronic rhinosinusitis: an immune barrier hypothesis.American journal of rhinologyReview
- Altered expression of genes associated with innate immunity and inflammation in recalcitrant rhinosinusitis with polyps.American journal of rhinologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a fungal etiology has been proposed to underlie severe nasal polyposis, the present study was undertaken to assess local antifungal immune reactivity in nasal polyposis. For this purpose, microbial colonization, along with the pattern of T helper 1 (Th1)/Th2 cytokine production and Toll-like receptor (TLR) expression, was evaluated in patients with nasal symptoms and with and without polyposis and in healthy subjects. The results show that Th2 reactivity was a common finding for patients with nasal polyposis regardless of the presence of microbes. The production of interleukin-10 was elevated in patients with bacterial and, particularly, fungal colonization, while both TLR2 expression and TLR4 expression were locally impaired in microbe-colonized patients. Eosinophils and neutrophils, highly recruited in nasal polyposis, were found to exert potent antifungal effector activities toward conidia and hyphae of the fungus and to be positively regulated by TLR2 or TLR4 stimulation. Therefore, a local imbalance between activating and deactivating signals to effector cells may likely contribute to fungal pathogenicity and the expression of local immune reactivity in nasal polyposis.
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What OpenQuestion holds
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.