Evidence map›Paper›PMID 22064707›Full record

ReviewImmunology and cell biology2012

Insights into inflammatory bowel disease using Toxoplasma gondii as an infectious trigger.

Charlotte E Egan, Sara B Cohen, Eric Y Denkers

Open access · bronzeAbstract readReview
In one paragraph

Review in Immunology and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-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

48 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
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  13. Nitric oxide in parasitic infections: a friend or foe?Journal of parasitic diseases : official organ of the Indian Society for Parasitology · 2022
    Review
  14. Mitigation ofJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2022
    Article
  15. Review
  16. Review
  17. ChronicProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Review
  19. Frontiers in psychiatry · 2021
    Review
  20. From Initiators to Effectors: Roadmap Through the Intestine During Encounter ofFrontiers in cellular and infection microbiology · 2020
    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

3 authors at 1 institution in 1 country.

Charlotte E EganDepartment of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Sara B Cohen
Eric Y Denkers
Cornell University · US

Funding

Role of intraepithelial T cells in Toxoplasma gondii-induced inflammatory ileitisR21AI083526 · NIAID · CORNELL UNIVERSITY · PI DENKERS, ERIC Y · 2009 to 2010
$422k
Role of CCL2/MCP-1 in mucosal immunity to ToxoplasmaR21AI068492 · NIAID · CORNELL UNIVERSITY · PI DENKERS, ERIC Y · 2007 to 2008
$418k
NIAID NIH HHS AI083526NIAID NIH HHS R21 AI068492NIAID NIH HHS R21 AI083526
6 · The paper itself

Abstract

Oral infection of certain inbred mouse strains with the protozoan Toxoplasma gondii triggers inflammatory pathology resembling lesions seen during human inflammatory bowel disease, in particular Crohn's disease (CD). Damage triggered by the parasite is largely localized to the distal portion of the small intestine, and as such is one of only a few models for ileal inflammation. This is important because ileal involvement is a characteristic of CD in over two-thirds of patients. The disease induced by Toxoplasma is mediated by Th1 cells and the cytokines tumor necrosis factor-α and interferon-γ. Inflammation is dependent upon IL-23, also identified by genome-wide association studies as a risk factor in CD. Development of lesions is concomitant with emergence of E. coli that display enhanced adhesion to the intestinal epithelium and subepithelial translocation. Furthermore, depletion of gut flora renders mice resistant to Toxoplasma-triggered ileitis. Recent findings suggest complex CCR2-dependent interactions between lamina propria T cells and intraepithelial lymphocytes in fueling proinflammatory pathology in the intestine. The advantage of the Toxoplasma model is that disease develops rapidly (within 7-10 days of infection) and can be induced in immunodeficient mice by adoptive transfer of mucosal T cells from infected donors. We propose that Toxoplasma acts as a trigger setting into motion a series of events culminating in loss of tolerance in the intestine and emergence of pathogenic T cell effectors. The Toxoplasma trigger model is providing new leaps in our understanding of immunity in the intestine.

Indexed as

Disease Models, AnimalAnimalsCytokinesHumansIleitisInflammatory Bowel DiseasesMiceModels, ImmunologicalReceptors, CCR2ToxoplasmaToxoplasmosis, AnimalCcr2 protein, mouseCytokinesReceptors, CCR2

Identifiers

PMID22064707
PMCPMC4094106
OpenAlexW2055769360

What OpenQuestion holds

Textmetadata
LicenceTDM
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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.