Evidence map›Paper›PMID 28833704›Full record

ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2017

Lipopolysaccharide suppresses IgE-mast cell-mediated reactions.

N Wang, M McKell, A Dang, A Yamani, L Waggoner, S Vanoni, T Noah, D Wu, A Kordowski, J Köhl and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 16 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 2 institutions in 3 countries.

N WangDivision of Allergy and Immunology, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
M McKellDivision of Immunobiology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
A DangDivision of Allergy and Immunology, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
A YamaniDivision of Allergy and Immunology, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
L WaggonerDivision of Allergy and Immunology, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
S VanoniDivision of Allergy and Immunology, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
T NoahDivision of Allergy and Immunology, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
D WuDivision of Allergy and Immunology, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
A KordowskiInstitute for Systemic Inflammation Research, University of Lübeck, Lübeck, Germany.
J KöhlDivision of Immunobiology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
K HoebeDivision of Immunobiology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
S DivanovicDivision of Immunobiology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
S P HoganDivision of Allergy and Immunology, University of Cincinnati College of Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.ORCID http://orcid.org/0000-0001-5793-4304
Cincinnati Children's Hospital Medical Center · USUniversity of Lübeck · DE

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
Immunology/Allergy Fellowship Training GrantT32AI060515 · NIAID · UNIVERSITY OF CINCINNATI · PI BERNSTEIN, DAVID I., ROTHENBERG, MARC E. · 2004 to 2018
$2.8M
Food Allergy and Goblet Cell Antigen PassagesR01AI112626 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOGAN, SIMON PATRICK, NEWBERRY, RODNEY D · 2015 to 2019
$2.4M
Pro-Type 2 Goblet Cell Antigen Passages in Food Sensitization and ReactivityR37AI112626 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SIMON Patrick HOGAN, Rodney D Newberry · 2023 to 2026
$2.2M
Interleukin-9 In Experimental Intestinal AnaphylaxisR01AI073553 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI HOGAN, SIMON PATRICK · 2008 to 2011
$1.5M
Eosinophil:M2 Macrophage:CCL11 Axis in Experimental Colitis and Pediatric CorticoR01DK090119 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI HOGAN, SIMON PATRICK · 2012 to 2015
$1.3M
NIAID NIH HHS R01 AI073553NIAID NIH HHS R01 AI112626NIAID NIH HHS R37 AI112626NIAID NIH HHS T32 AI060515NIDDK NIH HHS P30 DK078392NIDDK NIH HHS R01 DK090119
6 · The paper itself

Abstract

backgroundClinical and experimental analyses have identified a central role for IgE/FcεRI/mast cells in promoting IgE-mediated anaphylaxis. Recent data from human studies suggest that bacterial infections can alter susceptibility to anaphylaxis.

objectiveWe examined the effect of LPS exposure on the induction of IgE-mast cell (MC) mediated reactions in mice.

methodsC57BL/6 WT, tlr4

resultsWe show that LPS exposure of C57BL/6 WT mice constraints IgE-MC-mediated reactions. LPS-induced suppression of IgE-MC-mediated responses was TLR-4-dependent and associated with increased systemic IL-10 levels, decreased surface expression of FcεRI on MCs and loss of sensitivity to IgE activation. Notably, LPS-induced desensitization of MCs was short term with MC sensitivity to IgE reconstituted within 48 hours, which was associated with recapitulation of FcεRI expression on the MCs. Mechanistic analyses revealed a requirement for IL-10 in LPS-mediated decrease in MC FcεRI surface expression. CONCLUSIONS & CLINICAL RELEVANCE: Collectively, these studies suggest that LPS-induced IL-10 promotes the down-regulation of MC surface FcεRI expression and leads to desensitization of mice to IgE-mediated reactions. These studies indicate that targeting of the LPS-TLR-4-IL-10 pathway may be used as a therapeutic approach to prevent adverse IgE-mediated reactions.

Indexed as

AnaphylaxisAnimalsCalciumCell DegranulationDisease Models, AnimalGene Expression RegulationHematocritImmunoglobulin EInterleukin-10LipopolysaccharidesMacrophages, PeritonealMast CellsMiceMice, KnockoutReceptors, IgESignal TransductionCalciumImmunoglobulin EInterleukin-10LipopolysaccharidesReceptors, IgEToll-Like Receptor 4anaphylaxisIgEinnate immunity and TLR-4 signallingmast cells

Identifiers

PMID28833704
PMCPMC5865592
OpenAlexW2746541730

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.