Evidence map›Paper›PMID 31632299›Full record

ArticleFrontiers in physiology2019

Bitter Taste Receptors (TAS2Rs) in Human Lung Macrophages: Receptor Expression and Inhibitory Effects of TAS2R Agonists.

Stanislas Grassin-Delyle, Hélène Salvator, Nikola Mantov, Charlotte Abrial, Marion Brollo, Christophe Faisy, Emmanuel Naline, Louis-Jean Couderc, Philippe Devillier

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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  12. A deadly taste: linking bitter taste receptors and apoptosis.Apoptosis : an international journal on programmed cell death · 2025
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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

9 authors at 2 institutions in 1 country.

Stanislas Grassin-DelyleDepartment of Airway Diseases, Foch Hospital, Suresnes, France.
Hélène SalvatorDepartment of Airway Diseases, Foch Hospital, Suresnes, France.
Nikola MantovLaboratory of Research in Respiratory Pharmacology-UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay, Suresnes, France.
Charlotte AbrialLaboratory of Research in Respiratory Pharmacology-UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay, Suresnes, France.
Marion BrolloLaboratory of Research in Respiratory Pharmacology-UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay, Suresnes, France.
Christophe FaisyLaboratory of Research in Respiratory Pharmacology-UPRES EA 220, Foch Hospital, University Versailles Saint-Quentin, University of Paris-Saclay, Suresnes, France.
Emmanuel NalineDepartment of Airway Diseases, Foch Hospital, Suresnes, France.
Louis-Jean CoudercDepartment of Airway Diseases, Foch Hospital, Suresnes, France.
Philippe DevillierDepartment of Airway Diseases, Foch Hospital, Suresnes, France.
Université de Versailles Saint-Quentin-en-Yvelines · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBitter-taste receptors (TAS2Rs) are involved in airway relaxation but are also expressed in human blood leukocytes. We studied TAS2R expression and the effects of TAS2R agonists on the lipopolysaccharide (LPS)-induced cytokine release in human lung macrophages (LMs).

methodsLung macrophages were isolated from patients undergoing surgery for carcinoma. We used RT-qPCR to measure transcripts of 16 TAS2Rs (TAS2Rs 3/4/5/7/8/9/10/14/19/20/31/38/39/43/45 and 46) in unstimulated and LPS-stimulated (10 ng.mL

resultsThe transcripts of all 16 TAS2Rs were detected in macrophages. The addition of LPS led to an increase in the expression of most TAS2Rs, which was significant for TAS2R7 and 38. Although the promiscuous TAS2R agonists, quinine and denatonium, inhibited the LPS-induced release of TNF-α, CCL3 and CXCL8, diphenidol was inactive. Partially selective agonists (dapsone, colchicine, strychnine, and chloroquine) and selective agonists [erythromycin (TAS2R10), phenanthroline (TAS2R5), ofloxacin (TAS2R9), and carisoprodol (TAS2R14)] also suppressed the LPS-induced cytokine release. In contrast, two other agonists [sodium cromoglycate (TAS2R20) and saccharin (TAS2R31 and 43)] were inactive. TAS2R agonists suppressed IL-10 production - suggesting that this anti-inflammatory cytokine is not involved in the inhibition of cytokine production.

conclusionHuman LMs expressed TAS2Rs. Experiments with TAS2R agonists' suggested the involvement of TAS2Rs 3, 4, 5, 9, 10, 14, 30, 39 and 40 in the inhibition of cytokine production. TAS2Rs may constitute new drug targets in inflammatory obstructive lung disease.

Indexed as

bitter taste receptorcytokinehuman lung macrophageinflammationparenchyma explant

Identifiers

PMID31632299
PMCPMC6783802
OpenAlexW2970012271

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Registered trials

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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.