Evidence map›Paper›PMID 24556508›Full record

ArticlePeptides2014

Inflammation-induced functional connectivity of melanin-concentrating hormone and IL-10.

Dimitrios C Ziogas, Apostolos K A Karagiannis, Brenda M Geiger, Beatriz Gras-Miralles, Robert Najarian, Ofer Reizes, Leo R Fitzpatrick, Efi Kokkotou

Open access · greenAbstract read
In one paragraph

Article in Peptides, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 46% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. PDGF Promotes Dermal Fibroblast ActivationFrontiers in immunology · 2021
    Article
  3. Article
  4. Article
  5. Article
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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

8 authors at 4 institutions in 1 country.

Dimitrios C ZiogasDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States.
Apostolos K A KaragiannisDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States.
Brenda M GeigerDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States.
Beatriz Gras-MirallesDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States.
Robert NajarianDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States.
Ofer ReizesCleveland Clinic Foundation Lerner Research Institute, Cleveland, OH 44195, United States.
Leo R FitzpatrickPenn State College of Medicine, Hershey, PA 17036, United States.
Efi KokkotouDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States. Electronic address: ekokkoto@bidmc.harvard.edu.
Harvard University · USBeth Israel Deaconess Medical Center · USCleveland Clinic · USPenn State Milton S. Hershey Medical Center · US

Funding

Melanin-Concentrating Hormone as a Novel Mediator of Intestinal InflammationR01DK080058 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KOKKOTOU, EFI G. · 2008 to 2012
$1.6M
NIDDK NIH HHS DK080058NIDDK NIH HHS R01 DK080058
6 · The paper itself

Abstract

Melanin-concentrating hormone (MCH) was identified in mammals as a hypothalamic neuropeptide regulating appetite and energy balance. However, similarly to most of the brain peptides, MCH is also produced in the gastrointestinal system and can act locally as an immunomodulator. We have previously reported high expression of MCH and its receptor MCHR1 in the affected mucosa of patients with inflammatory bowel disease. Furthermore, MCH deficiency in mice attenuated experimental colitis, pointing to MCH as a mediator of intestinal inflammation. In the present study, in order to gain further insights into the underlying mechanisms of such effects of MCH, we treated mice with established experimental colitis due to IL-10 deficiency with a MCHR1 antagonist (DABA-822). While treatment with the same drug was successful in attenuating TNBS-induced colitis in previous studies, it offered no benefit to the IL-10 knockout mouse model, suggesting that perhaps IL-10 is a downstream target of MCH. Indeed, in experiments focusing on monocytes, we found that treatment with MCH inhibited LPS-mediated IL-10 upregulation. Conversely, in the same cells, exogenous IL-10 prevented LPS-induced MCHR1 expression. Taken together, these findings indicate a functional cross-talk between MCH and IL-10 which prevents resolution of inflammation.

Indexed as

AnimalsAnti-Inflammatory AgentsCell LineColitisGene ExpressionHypothalamic HormonesInterleukin-10LipopolysaccharidesMaleMelaninsMice, 129 StrainMice, Inbred C57BLMice, KnockoutPiroxicamPituitary HormonesReceptors, SomatostatinAnti-Inflammatory AgentsHypothalamic HormonesInterleukin-10LipopolysaccharidesMchr1 protein, mousemelanin-concentrating hormoneMelaninsPiroxicamPituitary HormonesReceptors, SomatostatinCytokinesIL-10Intestinal inflammationMelanin-concentrating hormoneMonocytesNeuropeptides

Identifiers

PMID24556508
PMCPMC4004662
OpenAlexW2017597546

What OpenQuestion holds

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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.