Evidence map›Paper›PMID 41768524›Full record

ArticleGastro hep advances2026

Loss of Nonhematopoietic Osteopontin Weakens the Intestinal Barrier and Alters the Microbiome and Metabolome in Mice.

Takehiro Hirano, Kohei Wagatsuma, Yuta Shimomori, Kotaro Akita, Tomoya Nakamura, Tsukasa Yamakawa, Yoshihiro Yokoyama, Hiroki Kurumi, Keisuke Ishigami, Kanna Nagaishi and 1 more

Abstract read
In one paragraph

Article in Gastro hep advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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

11 authors.

Takehiro HiranoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Kohei WagatsumaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Yuta ShimomoriDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Kotaro AkitaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Tomoya NakamuraDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Tsukasa YamakawaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Yoshihiro YokoyamaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Hiroki KurumiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Keisuke IshigamiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Kanna NagaishiDivision of Functional Morphology, Department of Anatomy, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.
Hiroshi NakaseDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Aims: Inflammatory bowel disease (IBD) is characterized by intestinal barrier disruption and dysregulated interactions between host immunity and gut microbiota. Osteopontin (OPN) is considered a proinflammatory mediator in IBD, but nonhematopoietic cell-derived OPN may exert barrier-protective functions. This study aimed to determine the effects of OPN in a murine model of acute colitis. Methods: We examined wild-type and OPN knockout mice under steady-state conditions and in dextran sulfate sodium-induced colitis, including bone marrow chimeras to distinguish the effects of hematopoietic and nonhematopoietic OPN. Results: Overt colitis did not occur under steady-state conditions. Compared with wild-type mice, OPN knockout mice exhibited crypt elongation, goblet cell hyperplasia, and increased epithelial proliferation. Gene expression analysis revealed reduced interleukin (IL)-22, IL-23, and IL-13 levels alongside increased interferon-γ, IL-1β, and IL-17A levels. 16S rRNA sequencing revealed increased alpha diversity, expansion of Conclusion: These findings indicate that nonhematopoietic cell-derived "guardian-type" OPN preserves barrier integrity, sustains IL-22/IL-23 production, and maintains microbiota-metabolome balance, whereas its loss induces a preinflammatory state that predisposes to acute mucosal injury. These findings provide a conceptual basis for stage- and source-specific therapeutic strategies in IBD.

Indexed as

Gut MicrobiotaInflammatory Bowel DiseaseInterleukin-22Intestinal BarrierOsteopontin

Identifiers

PMID41768524
PMCPMC12938857

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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.