Evidence map›Paper›PMID 30105015›Full record

ArticleFrontiers in immunology2018

C-Reactive Protein Stimulates Nicotinic Acetylcholine Receptors to Control ATP-Mediated Monocytic Inflammasome Activation.

Katrin Richter, Sabrina Sagawe, Andreas Hecker, Mira Küllmar, Ingolf Askevold, Jelena Damm, Sarah Heldmann, Michael Pöhlmann, Sophie Ruhrmann, Michael Sander and 10 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.2field-weighted citation impact, top 11% 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, 50 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

20 authors at 4 institutions in 2 countries.

Katrin RichterLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Sabrina SagaweLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Andreas HeckerLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Mira KüllmarLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Ingolf AskevoldLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Jelena DammLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Sarah HeldmannLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Michael PöhlmannDepartment of Anesthesiology and Intensive Care Medicine, Justus-Liebig-University Giessen, Giessen, Germany.
Sophie RuhrmannDepartment of Anesthesiology and Intensive Care Medicine, Justus-Liebig-University Giessen, Giessen, Germany.
Michael SanderDepartment of Anesthesiology and Intensive Care Medicine, Justus-Liebig-University Giessen, Giessen, Germany.
Klaus-Dieter SchlüterPhysiological Institute, Justus-Liebig-University Giessen, Giessen, Germany.
Sigrid WilkerLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Inke R KönigInstitute of Medical Biometry and Statistics, University of Luebeck, Luebeck, Germany.
Wolfgang KummerInstitute of Anatomy and Cell Biology, Justus-Liebig-University Giessen, German Centre for Lung Research, Giessen, Germany.
Winfried PadbergLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Arik J HoneDepartment of Biology, University of Utah, Salt Lake City, UT, United States.
J Michael McIntoshDepartment of Biology, University of Utah, Salt Lake City, UT, United States.
Anna Teresa ZakrzewiczLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Christian KochDepartment of Anesthesiology and Intensive Care Medicine, Justus-Liebig-University Giessen, Giessen, Germany.
Veronika GrauLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, Justus-Liebig-University Giessen, German Centre for Lung Research (DZL), Giessen, Germany.
Justus-Liebig-Universität Gießen · DEGeorge E. Wahlen Department of VA Medical Center · USGerman Center for Lung Research · DEUniversity of Utah · US

Funding

Venoms, Biological Resources, Molecular BiologyP01GM048677 · NIGMS · UNIVERSITY OF UTAH · PI OLIVERA, BALDOMERO M · 1993 to 2018
$32.2M
Novel nAChR-Targeted PeptidesR01GM103801 · NIGMS · UNIVERSITY OF UTAH · PI MCINTOSH, J MICHAEL · 2012 to 2019
$2.4M
NIGMS NIH HHS P01 GM048677NIGMS NIH HHS R01 GM103801
6 · The paper itself

Abstract

Blood levels of the acute phase reactant C-reactive protein (CRP) are frequently measured as a clinical marker for inflammation, but the biological functions of CRP are still controversial. CRP is a phosphocholine (PC)-binding pentraxin, mainly produced in the liver in response to elevated levels of interleukin-1β (IL-1β) and of the IL-1β-dependent cytokine IL-6. While both cytokines play important roles in host defense, excessive systemic IL-1β levels can cause life-threatening diseases such as trauma-associated systemic inflammation. We hypothesized that CRP acts as a negative feedback regulator of monocytic IL-1β maturation and secretion. Here, we demonstrate that CRP, in association with PC, efficiently reduces ATP-induced inflammasome activation and IL-1β release from human peripheral blood mononuclear leukocytes and monocytic U937 cells. Effective concentrations are in the range of marginally pathologic CRP levels (IC

Indexed as

InflammationAdultAgedBiomarkersCells, CulturedC-Reactive ProteinCytokinesHumansInflammasomesInterleukin-1betaMaleMiddle AgedReceptors, NicotinicReceptors, Purinergic P2X7BiomarkersC-Reactive ProteinCytokinesInflammasomesInterleukin-1betaReceptors, NicotinicReceptors, Purinergic P2X7C-reactive proteininterleukin-1βmonocytesnicotinic acetylcholine receptorsNLRP3 inflammasomesterile inflammation

Identifiers

PMID30105015
PMCPMC6077200
OpenAlexW2885886016

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.