Evidence map›Paper›PMID 40761802›Full record

ArticleFrontiers in immunology2025

Sphingosine-1-phosphate alleviates colitis by regulating macrophage polarization and PI3k-Akt signaling.

Liang Hu, Zi Yang, Ying Zhang, Conglin Du, Yang Yang, Zhichao Chang, Xiangchun Li, Zhaochen Shan

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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
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.

Liang Hu *Outpatient Department of Oral and Maxillofacial Surgery, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
Zi Yang *Salivary Gland Disease Center and Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology and Beijing Laboratory of Oral Health, Capital Medical University, Beijing, China.
Ying ZhangOutpatient Department of Oral and Maxillofacial Surgery, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
Conglin DuSalivary Gland Disease Center and Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology and Beijing Laboratory of Oral Health, Capital Medical University, Beijing, China.
Yang YangSalivary Gland Disease Center and Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology and Beijing Laboratory of Oral Health, Capital Medical University, Beijing, China.
Zhichao ChangSalivary Gland Disease Center and Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology and Beijing Laboratory of Oral Health, Capital Medical University, Beijing, China.
Xiangchun LiDepartment of Stomatology, The First Hospital of Qinhuangdao, Hebei, China.
Zhaochen ShanOutpatient Department of Oral and Maxillofacial Surgery, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Inflammatory bowel disease (IBD) is a complex disease that is characterized by tight junction loss and dysregulation of immune homeostasis. The repair of intestinal integrity and immune function in IBD remains a clinical challenge. Sphingosine-1-phosphate (S1P) has been reported to alleviate radiation-induced salivary gland damage by maintaining epithelial integrity. However, its potential to restore function during IBD has not yet been investigated. Methods: Dextran sulfate sodium (DSS) was added to the drinking water of C57BL/6 mice for 5 days to induce colitis. Subsequently, S1P and vehicle were injected intravenously on days 1, 3, and 5. Body weight, the disease activity index (DAI), and the histological activity index (HAI) were recorded. The level of apoptosis and expression of tight junction proteins among the groups were compared. We explored the underlying mechanisms of S1P using RNA sequencing. Results: S1P alleviated DSS-induced colitis by suppressing inflammatory cell infiltration, reducing ulcers, and maintaining intestinal epithelial junction integrity by increasing E-cadherin and occludin expression. S1P decreased apoptosis, suppressed M1 macrophage polarization and promoted M2 macrophage polarizaion. RNA sequencing revealed upregulation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K-Akt) and chemokine signaling pathways in the DSS group compared with those in the S1P group. Conclusions: S1P alleviated colitis by maintaing the intestinal epithelial integrity, promoting the polarization of M2 macrophage, suppressing chemokines, and regulating PI3K/Akt signaling pathway.

Indexed as

ColitisLysophospholipidsMacrophage ActivationMacrophagesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSphingosineAnimalsApoptosisDextran SulfateDisease Models, AnimalIntestinal MucosaMaleMiceMice, Inbred C57BLSignal TransductionDextran SulfateLysophospholipidsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSphingosinesphingosine 1-phosphateinflammatory bowel diseaseintestinal epithelial integritymacrophagePI3K-Akt signaling pathwaysphingosine-1-phosphate

Identifiers

PMID40761802
PMCPMC12318956

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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.