Evidence map›Paper›PMID 42298184›Full record

Articlenpj biomedical innovations2026

In vitro modeling of inflammatory bowel diseases using a newly developed immunocompetent colon epithelial monolayer co-culture model.

Imen Larafa, Roxana Zogorean, Adrian Buehler, Claudia Günther, Stefan Wirtz, Markus F Neurath, Oana-Maria Thoma, Maximilian J Waldner

Abstract read
In one paragraph

Article in npj biomedical innovations, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Imen LarafaDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. imen.larafa@uk-erlangen.de.
Roxana ZogoreanDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Adrian BuehlerDepartment of Pediatrics and Adolescent Medicine, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Claudia GüntherDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Stefan WirtzDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Markus F NeurathDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Oana-Maria ThomaDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Maximilian J WaldnerDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical treatment of inflammatory bowel diseases (IBD) remains challenging due to the complex interplay between the epithelial barrier, immune system, and gut microbiota. While in vitro models are pivotal for studying barrier dysfunction, developing a standardized and functionally relevant system for IBD remains challenging. To overcome this, we established an immunocompetent murine colon epithelium monolayer to model IBD-like conditions. Colons from wild-type mice were digested into single cells and seeded onto Matrigel-coated transwells. Within seven days, monolayers showed strong barrier properties and displayed epithelial cell lineage, including goblet, stem, and enteroendocrine cells. However, exposure to pro-inflammatory cytokines as well as infection with pathogenic bacteria, including Clostridium rodentium and Salmonella Typhimurium, disrupted epithelial integrity. To better reflect the in vivo state, polarized T cells and macrophages were co-cultured with the epithelium. Pro-inflammatory Th1 and Th17 cells impaired barrier function, while M0 and M2 macrophages maintained it, representing both homeostatic and disrupted conditions of the gut. Upon Salmonella Typhimurium infection, M1 macrophages produced IFN-γ, and M2 macrophages secreted IL-10 and enhanced ZO-1 expression. Overall, our model presents a promising platform to study epithelial barrier dysfunction, immune-epithelial cross-talk, and host-pathogen interactions, offering valuable insights into IBD mechanisms and potential therapeutic approaches.

Identifiers

PMID42298184
PMCPMC13269889

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Registered trials

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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.