Evidence map›Paper›PMID 25487064›Full record

ArticleEuropean journal of immunology2015

Enterocolitis causes profound lymphoid depletion in endothelin receptor B- and endothelin 3-null mouse models of Hirschsprung-associated enterocolitis.

Philip K Frykman, Zhi Cheng, Xiao Wang, Deepti Dhall

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02193685 (Identification of Genetic, Immunologic and Microbial Markers of Hirschsprung Associated Enterocolitis in Children With Hirschsprung Disease), which is not on this map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 15% 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.

NCT02193685 unknown statusnot on this map

Identification of Genetic, Immunologic and Microbial Markers of Hirschsprung Associated Enterocolitis in Children With Hirschsprung Disease

TypeobservationalSponsorCedars-Sinai Medical CenterRan2010 to 2025Enrolled400ConditionsHirschsprung Disease, Enterocolitis
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Identification of immune-related hub genes in spinal cord injury.European journal of medical research · 2024
    Article
  5. Article
  6. Hirschsprung-associated enterocolitis: a comprehensive review.World journal of pediatric surgery · 2024
    Review
  7. Article
  8. Article
  9. Update on the Pathogenesis of the Hirschsprung-Associated Enterocolitis.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Molecular medicine reports · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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 at 1 institution in 1 country.

Philip K FrykmanDivision of Pediatric Surgery and The Pediatric Surgery Laboratory, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Zhi Cheng
Xiao Wang
Deepti Dhall
Cedars-Sinai Medical Center · US

Funding

ET3-EDNRB Signaling in Enterocolitis Associated with Colonic AganglionosisK08DK090281 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI FRYKMAN, PHILIP KENT · 2011 to 2015
$755k
NIDDK NIH HHS 1K08DK090281NIDDK NIH HHS K08 DK090281
6 · The paper itself

Abstract

Potentially life-threatening enterocolitis is the most frequent complication in children with colonic aganglionosis (Hirschsprung disease, HSCR), and little is known about the mechanisms leading to enterocolitis. Splenic lymphopenia has been reported in the Endothelin Receptor B (Ednrb)-null mouse model of HSCR that develops enterocolitis. In this study, we sought to identify molecular mechanisms underlying this immune phenotype. We employed the Ednrb(-/-) mouse, and the knockout of its ligand, Edn3 (Edn3(-/-)). The major finding is that enterocolitis in the Ednrb(-/-) and Edn3(-/-) mice lead to thymic involution, splenic lymphopenia, and suppression of B lymphopoiesis as a consequence of colonic aganglionosis, not an intrinsic Edn3-Ednrb signaling defect directly affecting the lymphoid organs. We showed that adoptive transfer of Ednrb(-/-) marrow repopulated the RAG2-null mice marrow, thymus and spleen without development of enterocolitis. We identified the glucocorticoid corticosterone, as a potential mediator of the immune phenotype. This previously unrecognized pattern of immune abnormalities in mouse is nearly identical to lymphoid depletion in neonatal sepsis during severe physiological stress, suggesting that the mouse model used here could be also used for sepsis studies.

Indexed as

AnimalsColonCorticosteroneDisease Models, AnimalEndothelin-3EnterocolitisHirschsprung DiseaseMiceMice, KnockoutReceptor, Endothelin BSpleenThymus GlandCorticosteroneEndothelin-3Receptor, Endothelin BCorticosteroneEndothelinsEnterocolitisGlucocorticoidsHAECHirschsprung diseaseLymphoid depletion

Identifiers

PMID25487064
PMCPMC4370321
OpenAlexW1594947163

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

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.