Evidence map›Paper›PMID 22238655›Full record

ArticlePloS one2012

Chronic rejection pathology after orthotopic lung transplantation in mice: the development of a murine BOS model and its drawbacks.

Stéphanie De Vleeschauwer, Wolfgang Jungraithmayr, Shana Wauters, Stijn Willems, Manuela Rinaldi, Annemie Vaneylen, Stijn Verleden, Anna Willems-Widyastuti, Ken Bracke, Guy Brusselle and 4 more

Open access · goldAbstract readEvaluation Study
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Fibrotic progression from acute cellular rejection is dependent on secondary lymphoid organs in a mouse model of chronic lung allograft dysfunction.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024
    Article
  2. Smoking exposure-induced bronchus-associated lymphoid tissue in donor lungs does not prevent tolerance induction after transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Update on Chronic Lung Allograft Dysfunction.Current transplantation reports · 2016
    Article
  12. Article
  13. CD4 T Cells but Not Th17 Cells Are Required for Mouse Lung Transplant Obliterative Bronchiolitis.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015
    Article
  14. Article
  15. Article
  16. Immune response to tissue-restricted self-antigens induces airway inflammation and fibrosis following murine lung transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2014
    Article
  17. Increased T cell glucose uptake reflects acute rejection in lung grafts.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2013
    Article
  18. Ferret lung transplant: an orthotopic model of obliterative bronchiolitis.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2013
    Article
  19. Complement activation is not required for obliterative airway disease induced by antibodies to major histocompatibility complex class I: Implications for chronic lung rejection.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2012
    Article
  20. T regulatory cells play a significant role in modulating MHC class I antibody-induced obliterative airway disease.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2012
    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

14 authors at 3 institutions in 2 countries.

Stéphanie De VleeschauwerLaboratory of Pneumology, Katholieke Universiteit Leuven, Leuven, Belgium.
Wolfgang Jungraithmayr
Shana Wauters
Stijn Willems
Manuela Rinaldi
Annemie Vaneylen
Stijn Verleden
Anna Willems-Widyastuti
Ken Bracke
Guy Brusselle
Erik Verbeken
Dirk Van Raemdonck
Geert Verleden
Bart Vanaudenaerde
KU Leuven · BEGhent University Hospital · BEUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Almost all animal models for chronic rejection (CR) after lung transplantation (LTx) fail to resemble the human situation. It was our attempt to develop a representative model of CR in mice. Orthotopic LTx was performed in allografts receiving daily immunosuppression with steroids and cyclosporine. Controls included isografts and mice only undergoing thoracotomy (SHAM). Allografts were sacrificed 2, 4, 6, 8, 10 or 12 weeks after LTx. Pulmonary function was measured repeatedly in the 12w allografts, isografts and SHAM mice. Histologically, all allografts demonstrated acute rejection (AR) around the blood vessels and airways two weeks after LTx. This decreased to 50-75% up to 10 weeks and was absent after 12 weeks. Obliterative bronchiolitis (OB) lesions were observed in 25-50% of the mice from 4-12 weeks. Isografts and lungs of SHAM mice were normal after 12 weeks. Pulmonary function measurements showed a decline in FEV(0.1), TLC and compliance in the allografts postoperatively (2 weeks) with a slow recovery over time. After this initial decline, lung function of allografts increased more than in isografts and SHAM mice indicating that pulmonary function measurement is not a good tool to diagnose CR in a mouse. We conclude that a true model for CR, with clear OB lesions in about one third of the animals, but without a decline in lung function, is possible. This model is an important step forward in the development of an ideal model for CR which will open new perspectives in unraveling CR pathogenesis and exploring new treatment options.

Indexed as

AnimalsBronchiolitis ObliteransChronic DiseaseDisease Models, AnimalGraft RejectionHumansLung TransplantationMaleMiceMice, Inbred BALB CMice, Inbred C57BLSyndromeTime FactorsTransplantation, Homologous

Identifiers

PMID22238655
PMCPMC3253086
OpenAlexW2023919621

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.