Evidence map›Paper›PMID 30944544›Full record

ArticleMediators of inflammation2019

How Adhesion Molecule Patterns Change While Neutrophils Traffic through the Lung during Inflammation.

Franziska M Konrad, Julia Wohlert, Jutta Gamper-Tsigaras, Kristian-Christos Ngamsri, Jörg Reutershan

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. The Role of Innate Immunity in Pulmonary Infections.BioMed research international · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

5 authors at 2 institutions in 1 country.

Franziska M KonradDepartment of Anesthesiology and Intensive Care Medicine, University Hospital of Tübingen, Tübingen, Germany.ORCID 0000-0002-9259-7232
Julia WohlertDepartment of Anesthesiology and Intensive Care Medicine, University Hospital of Tübingen, Tübingen, Germany.
Jutta Gamper-TsigarasDepartment of Anesthesiology and Intensive Care Medicine, University Hospital of Tübingen, Tübingen, Germany.
Kristian-Christos NgamsriDepartment of Anesthesiology and Intensive Care Medicine, University Hospital of Tübingen, Tübingen, Germany.
Jörg ReutershanDepartment of Anesthesiology and Intensive Care Medicine, Hospital of Bayreuth, Germany.ORCID 0000-0003-3408-8226
University Children's Hospital Tübingen · DEBayreuth Medical Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In acute pulmonary inflammation, polymorphonuclear cells (PMNs) pass a transendothelial barrier from the circulation into the lung interstitium followed by a transepithelial migration into the alveolar space. These migration steps are regulated differentially by a concept of adhesion molecules and remain-despite decades of research-incompletely understood. Current knowledge of changes in the expression pattern of adhesion molecules mainly derives from in vitro studies or from studies in extrapulmonary organ systems, where regulation of adhesion molecules differs significantly. In a murine model of lung inflammation, we determined the expression pattern of nine relevant neutrophilic adhesion molecules on their way through the different compartments of the lung. We used a flow cytometry-based technique that allowed describing spatial distribution of the adhesion molecules expressed on PMNs during their migration through the lung in detail. For example, the highest expression of CD29 was found in the intravascular compartment, highlighting its impact on the initial adhesion to the endothelium. CD47 showed its peak of expression on the later phase of transendothelial migration, whereas CD11b and CD54 expression peaked interstitial. A pivotal role for transepithelial migration was found for the adhesion molecule CD172a. Thereby, expression may correlate with functional impact for specific migration steps. In vitro studies further confirmed our in vivo findings. In conclusion, we are the first to determine the changes in expression patterns of relevant adhesion molecules on their migration through the different compartments of the lung. These findings may help to further understand the regulation of neutrophil trafficking in the lung.

Indexed as

Acute Lung InjuryAnimalsCD11b AntigenCD47 AntigenCell AdhesionCell Adhesion MoleculesFlow CytometryInflammationIntegrin beta1Intercellular Adhesion Molecule-1LipopolysaccharidesLungMaleMiceMice, Inbred C57BLNeutrophilsCD11b AntigenCD47 AntigenCell Adhesion MoleculesIntegrin beta1Intercellular Adhesion Molecule-1LipopolysaccharidesReceptors, ImmunologicSirpa protein, mouse

Identifiers

PMID30944544
PMCPMC6421765
OpenAlexW2919884162

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.