Evidence map›Paper›PMID 35924188›Full record

ArticleClinical & translational immunology2022

An autologous colonic organoid-derived monolayer model to study immune: bacterial interactions in Crohn's disease patients.

Hamish Ck Angus, Paulo Cm Urbano, Gemma A Laws, Shijun Fan, Safina Gadeock, Michael Schultz, Grant Butt, Andrew J Highton, Roslyn A Kemp

Open access · goldAbstract read
In one paragraph

Article in Clinical & translational immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  3. Ion transport and epithelial barrier dysfunction in experimental models of ulcerative colitis.American journal of physiology. Gastrointestinal and liver physiology · 2025
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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

9 authors at 2 institutions in 2 countries.

Hamish Ck AngusDepartment of Microbiology and Immunology University of Otago Dunedin New Zealand.
Paulo Cm UrbanoDepartment of Microbiology and Immunology University of Otago Dunedin New Zealand.
Gemma A LawsDepartment of Microbiology and Immunology University of Otago Dunedin New Zealand.
Shijun FanDepartment of Microbiology and Immunology University of Otago Dunedin New Zealand.
Safina GadeockDepartment of Physiology University of Otago Dunedin New Zealand.
Michael SchultzDepartment of Medicine University of Otago Dunedin New Zealand.
Grant ButtDepartment of Physiology University of Otago Dunedin New Zealand.
Andrew J HightonDepartment of Microbiology and Immunology University of Otago Dunedin New Zealand.
Roslyn A KempDepartment of Microbiology and Immunology University of Otago Dunedin New Zealand.ORCID https://orcid.org/0000-0001-9092-1150
University of Otago · NZUC San Diego Health System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Crohn's disease (CD) initiation and pathogenesis are believed to involve an environmental trigger in a genetically susceptible person that results in an immune response against commensal gut bacteria, leading to a compromised intestinal epithelial barrier and a cycle of inflammation. However, it has been difficult to study the contribution of all factors together in a physiologically relevant model and in a heterogenous patient population. Methods: We developed an autologous colonic monolayer model that incorporated the immune response from the same donor and a commensal bacteria, Results: Monolayers derived from CD donors had impaired epithelial integrity compared to those from non-inflammatory bowel disease (IBD) donors. This integrity was further impaired by culture with bacteria, but not immune cells, despite a higher frequency of inflammatory phenotype peripheral T cells in CD donors. Variability in epithelial integrity was higher in CD donors than in non-IBD donors. Conclusion: We have developed a new autologous model to study the complexity of CD, which allows for the comparison of the barrier properties of the colonic epithelium and the ability to study how autologous immune cells directly affect the colonic barrier and whether this is modified by luminal bacteria. This new model allows for the study of individual patients and could inform treatment decisions.

Indexed as

bacteriaCrohn's diseasecytokinesepitheliumorganoidT cells

Identifiers

PMID35924188
PMCPMC9342672
OpenAlexW4289275040

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.