Evidence map›Paper›PMID 41998248›Full record

ArticleScientific reports2026

Intestinal epithelial cell-specific deletion of Jak2 disrupts gut homeostasis.

Brooke D'Mello, Daniel Rivera, Sonia Rehal, Evan Pollock-Tahiri, Yu Zhe Li, David Dodington, Kay-Uwe Wagner, Catherine Streutker, Minna Woo

Abstract read
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In one paragraph

Article in Scientific reports, 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

9 authors.

Brooke D'Mello *University Health Network Research Institute, University Health Network, Toronto, ON, Canada.
Daniel Rivera *University Health Network Research Institute, University Health Network, Toronto, ON, Canada.
Sonia RehalUniversity Health Network Research Institute, University Health Network, Toronto, ON, Canada.
Evan Pollock-TahiriUniversity Health Network Research Institute, University Health Network, Toronto, ON, Canada.
Yu Zhe LiUniversity Health Network Research Institute, University Health Network, Toronto, ON, Canada.
David DodingtonUniversity Health Network Research Institute, University Health Network, Toronto, ON, Canada.
Kay-Uwe WagnerDepartment of Oncology, Wayne State University School of Medicine and Tumor Biology Program, Barbara Ann Karmanos Cancer Institute, Detroit, MI, 48201, USA.
Catherine StreutkerDepartment of Laboratory Medicine, Unity Health Toronto, Toronto, ON, Canada.
Minna WooUniversity Health Network Research Institute, University Health Network, Toronto, ON, Canada. Minna.woo@uhn.ca.

Funding

CIHR CIHR - PJT-159505Heart and Stroke Foundation of Canada HSFC - G 23 0035438
6 · The paper itself

Abstract

Disruption of the intestinal epithelial barrier is recognized as a driver of inflammatory bowel disease (IBD) pathogenesis, yet the signaling pathways that govern epithelial integrity remain incompletely defined. Among these, Janus kinase (JAK)-mediated signaling plays a role in intestinal epithelial cells (IECs), coordinating barrier function and host defense. However, the role of JAK2 in IECs remains poorly understood. To investigate the in vivo role of epithelial JAK2, we generated mice with IEC-specific Jak2 deletion using the Villin-Cre system. These mice were born at expected Mendelian ratios and normal body weights. By 12 weeks of age, they developed shortened colons and exhibited mild small intestinal inflammation under homeostatic conditions. Histological analysis revealed increased neutrophilic infiltration and epithelial damage in the small intestine, without overt colitis. JAK2 deficiency led to increased intestinal permeability, with altered expression of genes that determine tight junctions, and a skewed cytokine gene expression profile marked by elevated Il13 and Il17 and reduced Il1-β and Il6. When subjected to dextran sodium sulfate (DSS)-induced colitis, Jak2-deficient mice exhibited sex-dependent weight loss. These findings show that IEC-specific JAK2 promotes barrier integrity and constrains low-grade inflammation under homeostatic conditions, highlighting a previously underappreciated role for epithelial JAK2 in mucosal regulation.

Indexed as

ColitisEpithelial CellsHomeostasisIntestinal MucosaJanus Kinase 2AnimalsCytokinesDextran SulfateFemaleGene DeletionInflammatory Bowel DiseasesIntestinal Barrier FunctionMaleMiceMice, KnockoutSignal TransductionCytokinesDextran SulfateJak2 protein, mouseJanus Kinase 2ColitisInflammatory bowel diseaseIntestinal epithelial cellsIntestinal homeostasisJAK2

Identifiers

PMID41998248
PMCPMC13250147

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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.