Evidence map›Paper›PMID 28689792›Full record

ArticleThe Journal of allergy and clinical immunology2018

Functional role of kynurenine and aryl hydrocarbon receptor axis in chronic rhinosinusitis with nasal polyps.

Heng Wang, Danh C Do, Jinxin Liu, Baofeng Wang, Jingjing Qu, Xia Ke, Xiaoyan Luo, Ho Man Tang, Ho Lam Tang, Chengping Hu and 3 more

Abstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

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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

13 authors at 5 institutions in 2 countries.

Heng WangDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Md; Department of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Danh C DoDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Md.
Jinxin LiuDepartment of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Baofeng WangDepartment of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jingjing QuDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Md; Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, China.
Xia KeDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Md.
Xiaoyan LuoDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Md.
Ho Man TangInstitute for Basic Biomedical Sciences, Johns Hopkins University School of Medicine, Baltimore, Md.
Ho Lam TangDepartment of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md.
Chengping HuDepartment of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, China.
Mark E AndersonDepartment of Medicine, Johns Hopkins School of Medicine, Baltimore, Md.
Zheng LiuDepartment of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address: zhengliuent@hotmail.com.
Peisong GaoDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Md. Electronic address: pgao1@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · USTongji Hospital · CNCentral South University · CNHuazhong University of Science and Technology · CN

Funding

Mitochondrial Calmodulin Kinase II in Physiology and DiseaseR01HL070250 · NHLBI · VANDERBILT UNIVERSITY · PI ANDERSON, MARK E · 2002 to 2017
$5.2M
CaMKII in Sinus Node Physiology and DiseaseR01HL096652 · NHLBI · UNIVERSITY OF IOWA · PI ANDERSON, MARK E · 2009 to 2016
$3.0M
Sensitization to Cockroach Allergen: Immune Regulation and Genetic DeterminantsR01ES021739 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2013 to 2017
$1.8M
Mannose Receptor, miR-511-3p, and Macrophage Polarization in AsthmaR21AI121768 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2016 to 2017
$462k
Identification of Candidate Genes for Specific Immune Responsiveness to CockroachR21AI088406 · NIAID · JOHNS HOPKINS UNIVERSITY · PI BARNES, KATHLEEN C, GAO, PEISONG · 2010 to 2011
$449k
Lineage Commitment of Mesenchymal Stem Cell in Allergen-induced Airway RemodelingR21AI109062 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2014 to 2015
$446k
NHLBI NIH HHS R01 HL070250NHLBI NIH HHS R01 HL096652NIAID NIH HHS R21 AI088406NIAID NIH HHS R21 AI109062NIAID NIH HHS R21 AI121768NIEHS NIH HHS R01 ES021739
6 · The paper itself

Abstract

backgroundChronic rhinosinusitis with nasal polyps (CRSwNP) is associated with mast cell-mediated inflammation and heightened oxidant stress. Kynurenine (KYN), an endogenous tryptophan metabolite, can promote allergen-induced mast cell activation through the aryl hydrocarbon receptor (AhR).

objectivesWe sought to determine the role of the KYN/AhR axis and oxidant stress in mast cell activation and the development of CRSwNP.

methodsWe measured the expression of indoleamine 2,3-dioxygenase 1, tryptophan 2,3-dioxygenase, KYN, and oxidized calmodulin-dependent protein kinase II (ox-CaMKII) in nasal polyps and controls. KYN-potentiated ovalbumin (OVA)-induced ROS generation, cell activation, and ox-CaMKII expression were investigated in wild-type and AhR-deficient (AhR

resultsNasal polyps in CRSwNP showed an increased expression of indoleamine 2,3-dioxygenase 1, tryptophan2,3-dioxygenase, and KYN compared with controls. AhR was predominantly expressed in mast cells in nasal polyps. Activated mast cells and local IgE levels were substantially increased in eosinophilic polyps compared with noneosinophilic polyps and controls. Furthermore, KYN potentiated OVA-induced ROS generation, intracellular Ca

conclusionsThese studies support a potentially critical but previously unidentified function of the KYN/AhR axis in regulating IgE-mediated mast cell activation through ROS and ox-CaMKII in CRSwNP.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 2Chronic DiseaseEosinophilsHumansIndoleamine-Pyrrole 2,3,-DioxygenaseMast CellsMiceMice, KnockoutNasal PolypsReceptors, Aryl HydrocarbonReceptors, GlutamateRhinitisSignal TransductionSinusitisAHR protein, humanAhr protein, mouseBasic Helix-Loop-Helix ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 2IDO1 protein, humanIndoleamine-Pyrrole 2,3,-Dioxygenasekynurenine receptorReceptors, Aryl HydrocarbonReceptors, Glutamatearyl hydrocarbon receptor (AhR)calmodulin-dependent protein kinase II (CaMKII)Chronic rhinosinusitis with nasal polypskynureninemast cell

Identifiers

PMID28689792
PMCPMC5937692
OpenAlexW2733069545

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.