Evidence map›Paper›PMID 26940548›Full record

ArticleNature communications2016

Protection from septic peritonitis by rapid neutrophil recruitment through omental high endothelial venules.

Konrad Buscher, Huiyu Wang, Xueli Zhang, Paul Striewski, Benedikt Wirth, Gurpanna Saggu, Stefan Lütke-Enking, Tanya N Mayadas, Klaus Ley, Lydia Sorokin and 1 more

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

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.9field-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

53 citing papers in PubMed, 95 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

11 authors at 4 institutions in 2 countries.

Konrad BuscherInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster 48149, Germany.
Huiyu WangInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster 48149, Germany.
Xueli ZhangInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster 48149, Germany.
Paul StriewskiCells-in-Motion Cluster of Excellence, University of Muenster, Muenster 48149, Germany.
Benedikt WirthCells-in-Motion Cluster of Excellence, University of Muenster, Muenster 48149, Germany.
Gurpanna SagguCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Stefan Lütke-EnkingInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster 48149, Germany.
Tanya N MayadasCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Klaus LeyDivision of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
Lydia SorokinInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster 48149, Germany.
Jian SongInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster 48149, Germany.
Brigham and Women's Hospital · USHarvard University · USLa Jolla Institute for Immunology · USUniversity of Münster · DE

Funding

Myeloid cell interactions with T cells in atherosclerosisR01HL115232 · NHLBI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI LEY, KLAUS F. · 2012 to 2018
$3.2M
NHLBI NIH HHS R01 HL115232
6 · The paper itself

Abstract

Acute peritonitis is a frequent medical condition that can trigger severe sepsis as a life-threatening complication. Neutrophils are first-responders in infection but recruitment mechanisms to the abdominal cavity remain poorly defined. Here, we demonstrate that high endothelial venules (HEVs) of the greater omentum constitute a main entry pathway in TNFα-, Escherichia coli (E. coli)- and caecal ligation and puncture-induced models of inflammation. Neutrophil transmigration across HEVs is faster than across conventional postcapillary venules and requires a unique set of adhesion receptors including peripheral node addressin, E-, L-selectin and Mac-1 but not P-selectin or LFA-1. Omental milky spots readily concentrate intra-abdominal E. coli where macrophages and recruited neutrophils collaborate in phagocytosis and killing. Inhibition of the omental neutrophil response exacerbates septic progression of peritonitis. This data identifies HEVs as a clinically relevant vascular recruitment site for neutrophils in acute peritonitis that is indispensable for host defence against early systemic bacterial spread and sepsis.

Indexed as

AnimalsAntigens, LyCell Adhesion MoleculesEscherichia coliEscherichia coli InfectionsFemaleGene Expression RegulationGenes, Transgenic, SuicideMaleMiceMice, KnockoutNeutrophilsOmentumPeritonitisSepsisTumor Necrosis Factor-alphaAntigens, LyCell Adhesion MoleculesLy6G antigen, mouseTumor Necrosis Factor-alpha

Identifiers

PMID26940548
PMCPMC4785224
OpenAlexW2333544438

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.