Evidence map›Paper›PMID 25301381›Full record

ArticleNeuroimmunomodulation2015

Vasoactive intestinal peptide-deficient mice exhibit reduced pathology in trinitrobenzene sulfonic acid-induced colitis.

Catalina Abad, Gardenia Cheung-Lau, Anne-Claire Coûté-Monvoisin, James A Waschek

Abstract read
In one paragraph

Article in Neuroimmunomodulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Neuroimmune Interactions in the Intestine.Annual review of immunology · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Immunomodulatory Roles of PACAP and VIP: Lessons from Knockout Mice.Journal of molecular neuroscience : MN · 2018
    Review
  11. Article
  12. Review
  13. Potential roles of enteric glia in bridging neuroimmune communication in the gut.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Review
  14. Article
  15. The Role of Neuropeptides in Mouse Models of Colitis.Journal of molecular neuroscience : MN · 2016
    Review
  16. Review
  17. Article
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

4 authors.

Catalina AbadDepartment of Psychiatry, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, Calif., USA.
Gardenia Cheung-Lau
Anne-Claire Coûté-Monvoisin
James A Waschek

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
Stem CellsP30HD004612 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOOKHEIMER, SUSAN Y · 1985 to 2014
$19.5M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
VIP AND PACP ACTION IN CNS DEVELOPMENT AND INJURYP01HD006576 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DE VELLIS, JEAN · 1985 to 2006
$7.8M
NCI NIH HHS P30 CA016042NICHD NIH HHS HD04612NICHD NIH HHS P01 HD006576NICHD NIH HHS P30 HD004612NIDDK NIH HHS P30 DK041301NIDDK NIH HHS P30DK41301
6 · The paper itself

Abstract

objectivesVasoactive intestinal peptide (VIP) is an immunomodulatory neuropeptide with therapeutic properties in multiple murine models of inflammatory disease including the trinitrobenzene-sulfonic acid (TNBS)-colitis model of Crohn's disease. Understanding the spectrum of biological actions of endogenously produced VIP may help us dissect the complex and multifactorial pathogenesis of such inflammatory diseases. Our goal was to determine the contribution of endogenously produced VIP to TNBS-colitis by using VIP knockout (KO) mice.

methodsTNBS was intracolonically administered to wild-type (WT) and VIP KO mice, and weight loss and colitis were assessed over time. Colon histopathological changes and myeloperoxidase activities were analyzed and the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in colon and serum quantified. The proliferative response in vitro of splenocytes from TNBS WT and VIP KO administered mice to anti-CD3 and anti-CD28 was determined.

resultsVIP KO mice did not exhibit the predicted exacerbated response to TNBS. Instead, they developed a milder clinical profile than WT mice, with lower TNF-α and IL-6 levels. Such potential defects seem selective, because other parameters such as the histopathological scores and the cytokine levels in the colon did not differ between the two strains of mice. Moreover, splenocytes from TNBS-treated VIP KO mice exhibited an enhanced proliferative response to anti-CD3/CD28 stimulation in vitro.

conclusionChronic loss of VIP in mice leads to a disruption of certain but not all immunological compartments, corroborating recent findings that VIP KO mice exhibit reduced mortality in the lipopolysaccharide-induced endotoxemia model and attenuated clinical development of experimental autoimmune encephalomyelitis while developing robust T-cell responses.

Indexed as

AnimalsCell ProliferationColitisColonCytokinesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayGene Expression RegulationMiceMice, Inbred C57BLMice, KnockoutPeroxidaseRNA, MessengerTime FactorsT-LymphocytesTrinitrobenzenesulfonic AcidCytokinesPeroxidaseRNA, MessengerTrinitrobenzenesulfonic AcidVasoactive Intestinal Peptide

Identifiers

PMID25301381
PMCPMC4297532

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.