Evidence map›Paper›PMID 24531552›Full record

ArticleThe Journal of clinical investigation2014

Bitter and sweet taste receptors regulate human upper respiratory innate immunity.

Robert J Lee, Jennifer M Kofonow, Philip L Rosen, Adam P Siebert, Bei Chen, Laurel Doghramji, Guoxiang Xiong, Nithin D Adappa, James N Palmer, David W Kennedy and 3 more

Registry-linked trialAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02766959 (Bitter Taste and Allele-specific Expression of the Human TAS2R38 Gene), which is not on this map. Cited by 243 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
243citing papers in PubMed, 2 pooled it
29.9field-weighted citation impact, top 1% 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.

NCT02766959 completednot on this mapstarted 2016, after this paper: background citation

Bitter Taste and Allele-specific Expression of the Human TAS2R38 Gene

TypeobservationalSponsorMonell Chemical Senses CenterRan2016 to 2018Enrolled57ConditionsRhinosinusitisArmsObservational study
3 · Its place in the literature

Who cites it

243 citing papers in PubMed, 2 syntheses or guidelines pooled it, 406 citations in OpenAlex.

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183 more citing papers are in PubMed but not listed here.

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

13 authors at 4 institutions in 1 country.

Robert J Lee
Jennifer M Kofonow
Philip L Rosen
Adam P Siebert
Bei Chen
Laurel Doghramji
Guoxiang Xiong
Nithin D Adappa
James N Palmer
David W Kennedy
James L Kreindler
Robert F Margolskee
Noam A Cohen
University of Pennsylvania · USChildren's Hospital of Philadelphia · USMonell Chemical Senses Center · USVeterans Health Administration · US

Funding

The Role of T1r Taste Receptors in GustationR01DC003155 · NIDCD · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI MARGOLSKEE, ROBERT F. · 1998 to 2014
$5.2M
GUSTDUCIN PHOSPHODIESTERASE INTERACTION IN GUSTATIONR01DC003055 · NIDCD · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI MARGOLSKEE, ROBERT F. · 1996 to 2013
$4.6M
NIDCD NIH HHS DC03055NIDCD NIH HHS R01 DC003055NIDCD NIH HHS R01 DC003155
6 · The paper itself

Abstract

Bitter taste receptors (T2Rs) in the human airway detect harmful compounds, including secreted bacterial products. Here, using human primary sinonasal air-liquid interface cultures and tissue explants, we determined that activation of a subset of airway T2Rs expressed in nasal solitary chemosensory cells activates a calcium wave that propagates through gap junctions to the surrounding respiratory epithelial cells. The T2R-dependent calcium wave stimulated robust secretion of antimicrobial peptides into the mucus that was capable of killing a variety of respiratory pathogens. Furthermore, sweet taste receptor (T1R2/3) activation suppressed T2R-mediated antimicrobial peptide secretion, suggesting that T1R2/3-mediated inhibition of T2Rs prevents full antimicrobial peptide release during times of relative health. In contrast, during acute bacterial infection, T1R2/3 is likely deactivated in response to bacterial consumption of airway surface liquid glucose, alleviating T2R inhibition and resulting in antimicrobial peptide secretion. We found that patients with chronic rhinosinusitis have elevated glucose concentrations in their nasal secretions, and other reports have shown that patients with hyperglycemia likewise have elevated nasal glucose levels. These data suggest that increased glucose in respiratory secretions in pathologic states, such as chronic rhinosinusitis or hyperglycemia, promotes tonic activation of T1R2/3 and suppresses T2R-mediated innate defense. Furthermore, targeting T1R2/3-dependent suppression of T2Rs may have therapeutic potential for upper respiratory tract infections.

Indexed as

Immunity, InnateCalcium SignalingCells, CulturedCiliaEpithelial CellsGlucoseHumansNasal MucosaPseudomonas aeruginosaQuaternary Ammonium CompoundsReceptors, G-Protein-CoupledRhinitisSinusitisTaste Receptors, Type 2Tissue Culture TechniquesdenatoniumGlucoseQuaternary Ammonium CompoundsReceptors, G-Protein-Coupledtaste receptors, type 1Taste Receptors, Type 2

Identifiers

PMID24531552
PMCPMC3934184
OpenAlexW2036927671

What OpenQuestion holds

Textmetadata
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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.