Evidence map›Paper›PMID 40065221›Full record

ArticleBMC immunology2025

Using gut microbiota and non-targeted metabolomics techniques to study the effect of xylitol on alleviating DSS-induced inflammatory bowel disease in mice.

Peng Ma, Wen Sun, Chang Sun, Jiajun Tan, Xueyun Dong, Jiayuan He, Asmaa Ali, Min Chen, Leilei Zhang, Liang Wu and 1 more

Abstract read
In one paragraph

Article in BMC immunology, 2025. 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
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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

11 authors.

Peng Ma *Department of Anesthesiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, 212001, China.
Wen Sun *Department of Critical Care Medicine, Jurong Hospital Afliated to Jiangsu University, Zhenjiang, Jiangsu, 212400, China.
Chang SunDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, China.
Jiajun TanDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, China.
Xueyun DongDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, China.
Jiayuan HeHealth Testing Center, Zhenjiang Center for Disease Control and Prevention, Zhenjiang, 212002, China.
Asmaa AliDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, China.
Min ChenPublic Experiment and Service Center, Jiangsu University, Zhenjiang, 212013, China.
Leilei ZhangDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, China.
Liang WuDepartment of Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, China. wl_ujs@163.com.
Pingping WangDepartment of Laboratory Medicine, Taizhou Second People's Hospital, Taizhou, 225309, China. Wangpp0229@qq.com.

Funding

Jiangsu Province Traditional Chinese medicine science and technology development program MS2022126Zhenjiang Key R&D Project-Social Development SH2022083Zhenjiang Key R&D Project-Social Development SH2023073
6 · The paper itself

Abstract

backgroundInflammatory bowel disease (IBD) has become a global healthcare issue, with its incidence continuing to rise, but currently there is no complete cure. Xylitol is a widely used sweetener in various foods and beverages, but there is limited research on the effects of xylitol on IBD symptoms.

aimStudy on the effect of oral xylitol in improving intestinal inflammation and damage in IBD mice, further explore the mechanism of xylitol in alleviating IBD symptoms using intestinal microbiota and non-targeted metabolomics techniques.

methodsAn IBD mouse model was induced using sodium dextran sulfate (DSS). After 30 days of oral administration of xylitol, we assessed the disease activity index (DAI) scores of mice in each group. The expression levels of inflammatory factors in the colon tissues were measured using qPCR. Additionally, we examined the damage to the intestinal mucosa and tight junction structures through HE staining and immunohistochemical staining. Finally, the alterations in the gut microbiota of the mice were analyzed using 16S rDNA sequencing technology.The production of three main short-chain fatty acids (SCFAs, including acetate, propionic acid and butyric acid) in feces and the changes of serum metabolomics were measured by non-targeted metabolomics techniques.

resultsThe findings indicated that xylitol effectively mitigated weight loss and improved the DAI score in mice with IBD. Moreover, xylitol reduced the expressions of Caspase-1, IL-1β, and TNF-α in the colon tissue of the mice, and increased the expressions of ZO-1 and occludin in intestinal mucosal. Xylitol could enhance the variety of intestinal bacteria in IBD mice and influenced the abundance of different bacterial species. Additionally, metabolomic analysis revealed that oral xylitol increased the levels of three main SCFAs in the feces of IBD mice, while also impacting serum metabolites.

conclusionsOur findings suggest that xylitol can help improve IBD symptoms. Xylitol can improve the intestinal flora of IBD mice and increase the production of SCFAs to play an anti-inflammatory role and protect the mucosal tight junction barrier. These discoveries present a fresh prophylactic treatment of IBD. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

Gastrointestinal MicrobiomeInflammatory Bowel DiseasesMetabolomicsXylitolAnimalsColonDextran SulfateDisease Models, AnimalIntestinal MucosaMaleMiceMice, Inbred C57BLDextran SulfateXylitolGut microbiotaInflammationInflammatory bowel diseaseMetabolomicsTight junctionXylitol

Identifiers

PMID40065221
PMCPMC11892251

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.