Evidence map›Paper›PMID 40661945›Full record

ArticleFrontiers in immunology2025

Bone marrow mesenchymal stem cell-derived exosomes alleviate DSS-induced inflammatory bowel disease in mice through inhibiting intestinal epithelial cell pyroptosis via delivery of TSG-6.

Bihua Wu, Shuangyan Su, Xianyu Wang, Yuwei Li, Zhenghao Mei, Fenglin Lou, Le Guo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. 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
–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

11 citing papers in PubMed.

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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

7 authors.

Bihua WuDepartment of Medical Microbiology and Immunology, School of Basic Medical Sciences, Dali University, Dali, Yunnan, China.
Shuangyan SuDepartment of Medical Microbiology and Immunology, School of Basic Medical Sciences, Dali University, Dali, Yunnan, China.
Xianyu WangDepartment of General Surgery, School of Clinical Medicine, Dali University, Dali, Yunnan, China.
Yuwei LiDepartment of Medical Microbiology and Immunology, School of Basic Medical Sciences, Dali University, Dali, Yunnan, China.
Zhenghao MeiDepartment of Medical Microbiology and Immunology, School of Basic Medical Sciences, Dali University, Dali, Yunnan, China.
Fenglin LouDepartment of Medical Microbiology and Immunology, School of Basic Medical Sciences, Dali University, Dali, Yunnan, China.
Le GuoDepartment of Medical Microbiology and Immunology, School of Basic Medical Sciences, Dali University, Dali, Yunnan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Inflammatory bowel disease (IBD), characterized by chronic intestinal inflammation and epithelial barrier dysfunction, remains a therapeutic challenge due to the limitations of current treatments, including drug resistance and invasive surgical risks. Emerging evidence implicates intestinal epithelial cells (IECs) pyroptosis as a key contributor to IBD progression. Bone marrow mesenchymal stem cell exosomes (BMSCs-Exo) exhibit anti-inflammatory and tissue-reparative potential, yet the role of tumor necrosis factor-stimulated gene 6 (TSG-6), a critical anti-inflammatory mediator in BMSCs-Exo, in modulating pyroptosis and intestinal barrier integrity remains unexplored. This study investigates the role of TSG-6 contained in mesenchymal stem cell-derived exosomes (MSCs-Exo) in alleviating IBD by modulating the pyroptosis signaling pathway in IECs. Results: In this study, TSG-6-enriched BMSCs-Exo significantly alleviated intestinal inflammation and pyroptosis in murine IBD models. BMSCs-Exo administration reduced NLRP3 inflammasome activation, suppressed Caspase-1-mediated Gasdermin D (GSDMD) cleavage, and decreased pro-inflammatory cytokine release (IL-1β, IL-18). Notably, TSG-6 knockdown in BMSCs-Exo abolished these protective effects, confirming its essential role in blocking the NLRP3/Caspase-1/GSDMD axis. Furthermore, BMSCs-Exo restored intestinal barrier integrity by upregulating tight junction proteins (e.g., ZO-1, occludin) and reducing epithelial permeability. Conclusion: This study identifies TSG-6 as a pivotal mediator in BMSCs-Exo that disrupts pyroptosis-driven IBD pathogenesis by targeting NLRP3 inflammasome activation. The findings highlight BMSCs-Exo as a cell-free therapeutic strategy to mitigate intestinal inflammation and barrier damage, offering advantages over traditional MSCs-based therapies in safety and specificity. By elucidating the TSG-6/NLRP3 regulatory axis, this work provides a novel framework for developing exosome-engineered treatments for IBD and other pyroptosis-related inflammatory disorders.

Indexed as

Cell Adhesion MoleculesEpithelial CellsExosomesInflammatory Bowel DiseasesIntestinal MucosaMesenchymal Stem CellsPyroptosisAnimalsDextran SulfateDisease Models, AnimalInflammasomesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinCell Adhesion MoleculesDextran SulfateInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinTnfaip6 protein, mousebone marrow mesenchymal stem cellsexosomesinflammatory bowel diseaseintestinal epithelial cellspyroptosisTSG-6

Identifiers

PMID40661945
PMCPMC12256234

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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.