Evidence map›Paper›PMID 30222138›Full record

Trial reportThe Journal of clinical investigation2018

Inhibition of neogenin fosters resolution of inflammation and tissue regeneration.

Martin Schlegel, Andreas Körner, Torsten Kaussen, Urs Knausberg, Carmen Gerber, Georg Hansmann, Hulda Soffia Jónasdóttir, Martin Giera, Valbona Mirakaj

Erratum issuedOpen access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
3.7field-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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Hematopoietic Stem Cells and the Immune System in Development and Aging.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Sema7A is crucial for resolution of severe inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Article
  16. Article
  17. Common Polymorphisms in theFrontiers in cardiovascular medicine · 2021
    Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Martin SchlegelDepartment of Anesthesiology and Intensive Care Medicine, Molecular Intensive Care Medicine, University Hospital Tübingen, Eberhard-Karls University Tübingen, Tübingen, Germany.
Andreas KörnerDepartment of Anesthesiology and Intensive Care Medicine, Molecular Intensive Care Medicine, University Hospital Tübingen, Eberhard-Karls University Tübingen, Tübingen, Germany.
Torsten KaussenDepartment of Pediatric Cardiology and Critical Care, Pulmonary Vascular Research Center, Hannover Medical School, Hannover, Germany.
Urs KnausbergDepartment of Anesthesiology and Intensive Care Medicine, Molecular Intensive Care Medicine, University Hospital Tübingen, Eberhard-Karls University Tübingen, Tübingen, Germany.
Carmen GerberDepartment of Anesthesiology and Intensive Care Medicine, Molecular Intensive Care Medicine, University Hospital Tübingen, Eberhard-Karls University Tübingen, Tübingen, Germany.
Georg HansmannDepartment of Pediatric Cardiology and Critical Care, Pulmonary Vascular Research Center, Hannover Medical School, Hannover, Germany.
Hulda Soffia JónasdóttirCenter for Proteomics and Metabolomics, Leiden University Medical Center (LUMC), Leiden, Netherlands.
Martin GieraCenter for Proteomics and Metabolomics, Leiden University Medical Center (LUMC), Leiden, Netherlands.
Valbona MirakajDepartment of Anesthesiology and Intensive Care Medicine, Molecular Intensive Care Medicine, University Hospital Tübingen, Eberhard-Karls University Tübingen, Tübingen, Germany.
University Children's Hospital Tübingen · DELeiden University Medical Center · NLMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The resolution of inflammation is an active process that is coordinated by endogenous mediators. Previous studies have demonstrated the immunomodulatory properties of the axonal guidance proteins in the initial phase of acute inflammation. We hypothesized that the neuronal guidance protein neogenin (Neo1) modulates mechanisms of inflammation resolution. In murine peritonitis, Neo1 deficiency (Neo1-/-) resulted in higher efficacies in reducing neutrophil migration into injury sites, increasing neutrophil apoptosis, actuating PMN phagocytosis, and increasing the endogenous biosynthesis of specialized proresolving mediators, such as lipoxin A4, maresin-1, and protectin DX. Neo1 expression was limited to Neo1-expressing Ly6Chi monocytes, and Neo1 deficiency induced monocyte polarization toward an antiinflammatory and proresolving phenotype. Signaling network analysis revealed that Neo1-/- monocytes mediate their immunomodulatory effects specifically by activating the PI3K/AKT pathway and suppressing the TGF-β pathway. In a cohort of 59 critically ill, intensive care unit (ICU) pediatric patients, we found a strong correlation between Neo1 blood plasma levels and abdominal compartment syndrome, Pediatric Risk of Mortality III (PRISM-III) score, and ICU length of stay and mortality. Together, these findings identify a crucial role for Neo1 in regulating tissue regeneration and resolution of inflammation, and determined Neo1 to be a predictor of morbidity and mortality in critically ill children affected by clinical inflammation.

Indexed as

RegenerationAdolescentAnimalsChildChild, PreschoolHumansInfantInfant, NewbornInflammationIntra-Abdominal HypertensionMaleMiceMice, KnockoutMonocytesNerve Tissue ProteinsNeutrophil InfiltrationNEO1 protein, humanNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Cell SurfaceCellular immune responseImmunologyInflammationInnate immunityMonocytes

Identifiers

PMID30222138
PMCPMC6159953
OpenAlexW2890510235

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.