Evidence map›Paper›PMID 25051500›Full record

ArticlePloS one2014

Carboxypeptidase E modulates intestinal immune homeostasis and protects against experimental colitis in mice.

Florian Bär, Bandik Föh, René Pagel, Torsten Schröder, Heidi Schlichting, Misa Hirose, Susanne Lemcke, Antje Klinger, Peter König, Christian M Karsten and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
1.6field-weighted citation impact, top 19% 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, 27 citations in OpenAlex.

  1. Observational
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  10. The Role of Neuropeptide Y in the Nucleus Accumbens.International journal of molecular sciences · 2021
    Review
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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

15 authors at 2 institutions in 1 country.

Florian BärMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany; Institute of Anatomy, University of Lübeck, Lübeck, Germany.
Bandik FöhMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany.
René PagelMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany.
Torsten SchröderMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany.
Heidi SchlichtingMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany.
Misa HiroseDepartment of Dermatology, University Hospital Schleswig-Holstein, Lübeck, Germany.
Susanne LemckeDepartment of Dermatology, University Hospital Schleswig-Holstein, Lübeck, Germany.
Antje KlingerInstitute of Anatomy, University of Lübeck, Lübeck, Germany.
Peter KönigInstitute of Anatomy, University of Lübeck, Lübeck, Germany.
Christian M KarstenInstitute for Systemic Inflammation Research, University of Lübeck, Lübeck, Germany.
Jürgen BüningMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany.
Hendrik LehnertMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany.
Klaus FellermannMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany.
Saleh M IbrahimDepartment of Dermatology, University Hospital Schleswig-Holstein, Lübeck, Germany.
Christian SinaMedical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany.
University of Lübeck · DEUniversity Hospital Schleswig-Holstein · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enteroendocrine cells (EEC) produce neuropeptides, which are crucially involved in the maintenance of the intestinal barrier. Hence, EEC dysfunction is suggested to be involved in the complex pathophysiology of inflammatory bowel disease (IBD), which is characterized by decreased intestinal barrier function. However, the underlying mechanisms for EEC dysfunction are not clear and suitable models for a better understanding are lacking. Here, we demonstrate that Carboxypeptidase E (CPE) is specifically expressed in EEC of the murine colon and ileum and that its deficiency is associated with reduced intestinal levels of Neuropeptide Y (NPY) and Peptide YY (PYY), which are both produced by EEC. Moreover, cpe-/- mice exhibit an aggravated course of DSS-induced chronic colitis compared to wildtype littermates. In addition, we observed elevated mucosal IL-6 and KC transcript levels already at baseline conditions in cpe-/- mice. Moreover, supernatants obtained from isolated intestinal crypts of cpe-/- mice lead to increased IL-6 and KC expression in MODE-K cells in the presence of LPS. This effect was reversible by co-administration of recombinant NPY, suggesting a CPE mediated immunosuppressive effect in the intestines by influencing the processing of specific neuropeptides. In this context, the chemotaxis of bone marrow derived macrophages towards respective supernatants was enhanced. In conclusion, our data point to an anti-inflammatory role of CPE in the intestine by influencing local cytokine levels and thus regulating the migration of myeloid immune cells into the mucosa. These findings highlight the importance of EEC for intestinal homeostasis and propose EEC as potential therapeutic targets in IBD.

Indexed as

AnimalsCarboxypeptidase HCell MovementCells, CulturedChromogranin BColitisColonDextran SulfateHomeostasisHumansInflammatory Bowel DiseasesIntestinal MucosaMice, Inbred C57BLMyeloid CellsNeuropeptide YProtein TransportCarboxypeptidase HChromogranin BDextran SulfateNeuropeptide Y

Identifiers

PMID25051500
PMCPMC4106776
OpenAlexW1992391800

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.