Evidence map›Paper›PMID 27759044›Full record

ArticleScientific reports2016

Lipopolysaccharide-induced hemolysis: Evidence for direct membrane interactions.

Stephan Brauckmann, Katharina Effenberger-Neidnicht, Herbert de Groot, Michael Nagel, Christian Mayer, Jürgen Peters, Matthias Hartmann

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. 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
3.8field-weighted citation impact, top 6% 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, 46 citations in OpenAlex.

  1. Review
  2. Article
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  5. Article
  6. Review
  7. Frontiers in immunology · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
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  14. Article
  15. Article
  16. Immunotoxicity Considerations for Next Generation Cancer Nanomedicines.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019
    Review
  17. Article
  18. Review
  19. Review
  20. Hemolysis-induced Lung Vascular Leakage Contributes to the Development of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2018
    Article
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

7 authors at 2 institutions in 1 country.

Stephan BrauckmannKlinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Universität Duisburg-Essen, Germany.
Katharina Effenberger-NeidnichtInstitut für Physiologische Chemie, Universitätsklinikum Essen, Universität Duisburg-Essen, Germany.
Herbert de GrootInstitut für Physiologische Chemie, Universitätsklinikum Essen, Universität Duisburg-Essen, Germany.
Michael NagelInstitut für Physikalische Chemie, Universität Duisburg-Essen, Germany.
Christian MayerInstitut für Physikalische Chemie, Universität Duisburg-Essen, Germany.
Jürgen PetersKlinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Universität Duisburg-Essen, Germany.
Matthias HartmannKlinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Universität Duisburg-Essen, Germany.
University of Duisburg-Essen · DEEssen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While hemolysis in patients with sepsis is associated with increased mortality its mechanisms are unknown and Toll-like receptor (TLR)-4 mediated effects, complement-mediated hemolysis, or direct cell membrane effects are all conceivable mechanisms. In this study, we tested the hypotheses that toxic lipopolysaccharide (LPS) as well as non-toxic RS-LPS evokes hemolysis (1) by direct membrane effects, and (2) independent of the complement system and TLR-4 activation. We found, that incubation with LPS resulted in a marked time and concentration dependent increase of free hemoglobin concentration and LDH activity in whole blood and washed red cells. Red cell integrity was diminished as shown by decreased osmotic resistance, formation of schistocytes and rolls, and a decrease in red cell membrane stiffness. Non-toxic RS-LPS inhibited the LPS-evoked increase in TNF-α concentration demonstrating its TLR-4 antagonism, but augmented LPS-induced increase in supernatant hemoglobin concentration and membrane disturbances. Removal of plasma components in washed red cell assays failed to attenuate hemolysis. In summary, this study demonstrates direct physicochemical interactions of LPS with red cell membranes resulting in hemolysis under in vitro conditions. It might thus be hypothesized, that not all effects of LPS are mediated by TLR and may explain LPS toxicity in cells missing TLR.

Indexed as

Anemia, HemolyticCell Membrane PermeabilityCells, CulturedComplement System ProteinsErythrocyte MembraneErythrocytesHemoglobinsHemolysisHumansLipopolysaccharidesL-Lactate DehydrogenaseSepsisToll-Like Receptor 4Tumor Necrosis Factor-alphaComplement System ProteinsHemoglobinsLipopolysaccharidesL-Lactate DehydrogenaseTLR4 protein, humanToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID27759044
PMCPMC5069489
OpenAlexW2538141437

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.