Evidence map›Paper›PMID 27671548›Full record

ArticleInternational forum of allergy & rhinology2017

Role of the type I tumor necrosis factor receptor in inflammation-associated olfactory dysfunction.

Davi Sousa Garcia, Mengfei Chen, Amy K Smith, Paulo Roberto Lazarini, Andrew P Lane

Open access · greenAbstract read
In one paragraph

Article in International forum of allergy & rhinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Olfactory Loss in Rhinosinusitis: Mechanisms of Loss and Recovery.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Review
  7. International consensus statement on allergy and rhinology: Olfaction.International forum of allergy & rhinology · 2022
    Review
  8. Article
  9. Review
  10. Chitinase-Like Protein Ym2 (Chil4) Regulates Regeneration of the Olfactory Epithelium via Interaction with Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  11. Endotyping chronic rhinosinusitis based on olfactory cleft mucus biomarkers.The Journal of allergy and clinical immunology · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Davi Sousa GarciaDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
Mengfei ChenDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
Amy K SmithDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
Paulo Roberto LazariniDepartment of Otolaryngology, Santa Casa de Sao Paulo School of Medical Sciences, Sao Paulo, Brazil.
Andrew P LaneDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
Johns Hopkins Medicine · USJohns Hopkins University · USFaculdade de Ciências Médicas da Santa Casa de São Paulo · BR

Funding

Chronic rhinosinusitis-associated olfactory lossR01DC009026 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI LANE, ANDREW P · 2008 to 2015
$2.9M
NIDCD NIH HHS R01 DC009026
6 · The paper itself

Abstract

backgroundTo understand mechanisms of human olfactory dysfunction in chronic rhinosinusitis, an inducible olfactory inflammation (IOI) model has been utilized to chronically express inflammatory cytokines locally, resulting in neuronal loss, diminished odorant responses, and repressed olfactory regeneration. Knockout of the minor tumor necrosis factor α receptor 2 (TNFR2) was previously shown to partially rescue these olfactory changes. The purpose of current study was to investigate the role of the major TNF receptor, TNFR1, in chronic olfactory inflammation.

methodsTwo experimental groups of mice were studied: TNFR1 knockout in IOI background and TNFR1 knockout with allergen-induced inflammation. Olfactory function was assayed by electro-olfactogram (EOG), and olfactory tissue was processed for histology and immunohistochemical staining.

resultsTNF-α was dramatically induced in IOI-TNFR1 knockout mice, but the olfactory epithelium did not show inflammation. EOG responses were normal after either 2 or 8 weeks of TNF-α expression. Ovalbumin-sensitized TNFR1 knockout mice developed markedly diminished eosinophilic inflammatory infiltration.

conclusionGenetic deletion of TNFR1 completely blocks TNF-α-induced inflammation and reduces allergen-induced inflammation. Preserved EOG responses suggest a TNFR1-dependent mechanism of TNF-α-induced olfactory neuron dysfunction.

Indexed as

AllergensAlum CompoundsAnimalsFemaleHypersensitivityInflammationMaleMice, KnockoutNasal Lavage FluidNeuronsOlfaction DisordersOlfactory MucosaOvalbuminReceptors, Tumor Necrosis Factor, Type ITumor Necrosis Factor-alphaAllergensAlum Compoundsaluminum sulfateOvalbuminReceptors, Tumor Necrosis Factor, Type ITnfrsf1a protein, mouseTumor Necrosis Factor-alphaeosinophilsinflammationolfactory epitheliumTNF-alphaTNFR1transgenic mice

Identifiers

PMID27671548
PMCPMC5400011
OpenAlexW2524308677

What OpenQuestion holds

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Registered trials

None linked

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.