Evidence map›Paper›PMID 28404637›Full record

ArticleJournal of lipid research2017

Surfactant inhibits ATP-induced release of interleukin-1β via nicotinic acetylcholine receptors.

Sören Backhaus, Anna Zakrzewicz, Katrin Richter, Jelena Damm, Sigrid Wilker, Gabriele Fuchs-Moll, Mira Küllmar, Andreas Hecker, Ivan Manzini, Clemens Ruppert and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  10. Review
  11. Article
  12. Article
  13. Amyloid Beta Peptide (AβJournal of clinical medicine · 2020
    Article
  14. Review
  15. Article
  16. Biosurfactants: A Covid-19 Perspective.Frontiers in microbiology · 2020
    Article
  17. Article
  18. Phosphocholine-Modified Lipooligosaccharides ofMolecules (Basel, Switzerland) · 2018
    Article
  19. Article
  20. Review
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 2 countries.

Sören BackhausLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Anna ZakrzewiczLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Katrin RichterLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Jelena DammLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Sigrid WilkerLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Gabriele Fuchs-MollLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Mira KüllmarLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Andreas HeckerLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Ivan ManziniDepartment of Animal Physiology and Molecular Biomedicine, Justus-Liebig-University Giessen, Giessen, Germany.
Clemens RuppertMedical Clinic II, Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), German Center for Lung Research (DZL), Justus-Liebig-University Giessen, Giessen, Germany.
J Michael McIntoshDepartments of Biology and Psychiatry, University of Utah and George E. Wahlen Veterans Affairs Medical Center, Salt Lake City, UT.
Winfried PadbergLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany.
Veronika GrauLaboratory of Experimental Surgery, Department of General and Thoracic Surgery Justus-Liebig-University Giessen, Giessen, Germany Veronika.Grau@chiru.med.uni-giessen.de.
Justus-Liebig-Universität Gießen · DEGeorge E. Wahlen Department of VA Medical Center · 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

Interleukin (IL)-1β is a potent pro-inflammatory cytokine of innate immunity involved in host defense. High systemic IL-1β levels, however, cause life-threatening inflammatory diseases, including systemic inflammatory response syndrome. In response to various danger signals, the pro-form of IL-1β is synthesized and stays in the cytoplasm unless a second signal, such as extracellular ATP, activates the inflammasome, which enables processing and release of mature IL-1β. As pulmonary surfactant is known for its anti-inflammatory properties, we hypothesize that surfactant inhibits ATP-induced release of IL-1β. Lipopolysaccharide-primed monocytic U937 cells were stimulated with an ATP analog in the presence of natural or synthetic surfactant composed of recombinant surfactant protein (rSP)-C, palmitoylphosphatidylglycerol, and dipalmitoylphosphatidylcholine (DPPC). Both surfactant preparations dose-dependently inhibited IL-1β release from U937 cells. DPPC was the active constituent of surfactant, whereas rSP-C and palmitoylphosphatidylglycerol were inactive. DPPC was also effective in primary mononuclear leukocytes isolated from human blood. Experiments with nicotinic antagonists, siRNA technology, and patch-clamp experiments suggested that stimulation of nicotinic acetylcholine receptors (nAChRs) containing subunit α9 results in a complete inhibition of the ion channel function of ATP receptor, P2X7. In conclusion, the surfactant constituent, DPPC, efficiently inhibits ATP-induced inflammasome activation and maturation of IL-1β in human monocytes by a mechanism involving nAChRs.

Indexed as

1,2-DipalmitoylphosphatidylcholineAdenosine TriphosphateElectrophysiological PhenomenaHumansInterleukin-1betaLeukocytes, MononuclearProtein SubunitsPulmonary SurfactantsReceptors, NicotinicU937 Cells1,2-DipalmitoylphosphatidylcholineAdenosine TriphosphateInterleukin-1betaProtein SubunitsPulmonary SurfactantsReceptors, NicotinicCHRNA10CHRNA7CHRNA9dipalmitoylphosphatidylcholineinflammasomemonocytephosphatidylcholinepurinergic receptor P2X 7

Identifiers

PMID28404637
PMCPMC5454502
OpenAlexW2606036376

What OpenQuestion holds

Textmetadata
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.