Evidence map›Paper›PMID 27650657›Full record

ArticleThe Laryngoscope2017

The genetics of the bitter taste receptor T2R38 in upper airway innate immunity and implications for chronic rhinosinusitis.

Noam A Cohen

Abstract read
In one paragraph

Article in The Laryngoscope, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Olfactory receptors and human diseases.Cell and tissue research · 2025
    Review
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
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  13. Biomedicines · 2024
    Article
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  18. Article
  19. International journal of molecular sciences · 2022
    Article
  20. 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

1 author at 1 institution in 1 country.

Noam A CohenDepartment of Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, U.S.A.
Philadelphia VA Medical Center · US

Funding

Chronic Rhinosinusitis and genetics of bitter taste receptorsR01DC013588 · NIDCD · UNIVERSITY OF PENNSYLVANIA · PI COHEN, NOAM A · 2014 to 2018
$2.4M
Targeted genotyping and gene expression with the QuantStudio 12K FlexS10OD018125 · OD · MONELL CHEMICAL SENSES CENTER · PI REED, DANIELLE RENEE · 2015 to 2015
$185k
NIDCD NIH HHS R01 DC013588
6 · The paper itself

Abstract

objectiveChronic rhinosinusitis (CRS) refractory to therapeutic intervention may involve a particularly resistant infection known as a bacterial biofilm. Critical to biofilm formation is the microbial process of quorum sensing whereby microbes secrete factors that regulate the expression of microbial genes involved in biofilm formation, persistence, and virulence. Here, we review recent work demonstrating that the bitter taste receptor T2R38, expressed on the apical surface of the sinonasal epithelium, serves a sentinel role in eavesdropping on microbial quorum-sensing communications and regulates localized innate biocidal defenses. Furthermore, studies investigating whether cilia are necessary for T2R38 expression and function in the upper airway are presented.

methodsPrimary human sinonasal air-liquid interface cultures were used to elucidate cellular pathways responsive to quorum-sensing molecules, whereas clinical studies investigated the contribution of T2R38 polymorphisms to recalcitrant chronic rhinosinusitis.

resultsT2R38 is stimulated by acyl-homoserine lactones, gram-negative quorum-sensing molecules, and subsequently activates nitric oxide-dependent innate immune responses. The formation of mature cilia is necessary for T2R38 expression and function, and polymorphisms that underlie T2R38 functionality appear to be involved in susceptibility to upper respiratory infection and recalcitrant CRS.

conclusionTaste receptors are emerging as critical components of early-phase respiratory innate immunity, detecting molecules used by microbes to communicate and stimulating localized host defenses. Genetic polymorphisms are very common within the taste receptors, and recent linkage studies have demonstrated associations of taste receptor genetics with CRS. Lastly, ciliogenesis, which is often impacted in CRS, is critical for the functional expression of T2R38. LEVEL OF EVIDENCE: N/A. Laryngoscope, 127:44-51, 2017.

Indexed as

Immunity, InnateBiofilmsCells, CulturedChronic DiseaseCiliaFluorescent Antibody TechniqueGenotypeHumansMicroscopy, ConfocalMicroscopy, Electron, ScanningMucociliary ClearancePolymorphism, Single NucleotideReceptors, G-Protein-CoupledRespiratory Tract InfectionsRhinitisSinusitisReceptors, G-Protein-CoupledTaste Receptors, Type 2chronic rhinosinusitisciliahost-pathogen interactionsinterkingdom signalingT2R38

Identifiers

PMID27650657
PMCPMC5177547
OpenAlexW2523839899

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.