Evidence map›Paper›PMID 38322881›Full record

ArticleHeliyon2024

Sodium butyrate restricts neutrophils migration and NETs formation through reducing macrophage-derived CXCL16 in calculous cholecystitis.

Hongsuo Chen, Jing Wang, Qingyu Ji, Zhenyu Jiang

Abstract read
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Gut fungi exacerbates gallstone formation by activating neutrophil extracellular traps in the liver.Apoptosis : an international journal on programmed cell death · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Diabetic wounds and short-chain fatty acids.Journal of diabetes and metabolic disorders · 2025
    Review
  7. Microbial cell (Graz, Austria) · 2025
    Article
  8. 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

4 authors.

Hongsuo ChenDepartment of Gastroenterology, the Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, 014030, China.
Jing WangDepartment of Gastroenterology, the Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, 014030, China.
Qingyu JiDepartment of Radiology, the Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, 014030, China.
Zhenyu JiangDepartment of Gastroenterology, the Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, 014030, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Neutrophil extracellular traps (NETs) havebeen demonstrated to initiate gallstone formation. Cholecystitis is a common complication of gallstones. As short-chain fatty acids (SCFAs), Butyrate acid has anti-inflammatory effects and alleviates cholesterol gallstones. However, the role of Butyrate acid in NETs of calculous cholecystitis and the molecular mechanism remains unclear. The effect of Sodium butyrate on neutrophil migration and NETs formation involved in macrophages polarization and exosomalCXCL16 in calculous cholecystitis was explored in our study. Methods: The number of neutrophils and NETs, macrophages polarization and exosomal CXCL16 level were analyzed in clinic samples from patients. Exosomes were obtained and verified by gradient centrifugation, transmission electron microscopy, NanoSight analysis and Western blotting. Transwell, immunofluorescence and ELISA were used to detect neutrophil migration and NETs formation. Results: Our results demonstrated that a large number of neutrophils and NETs, as well as M1 macrophages and exosomal CXCL16, were found in the blood of gallstones patients, especially patients with acute calculous cholecystitis. Exosomal CXCL16 was upregulated in plasma of calculous cholecystitis patients or Lipopolysaccharide induced macrophages, and promoted neutrophil cell migration and NETs formation. Sodium butyrate reduced exosomal CXCL16 secretion through the inhibition of M1 macrophage polarization to suppress neutrophils migration and NETs formation. Conclusion: Our study suggested that Sodium butyrate may inhibit neutrophils migration and NETs formation to alleviate calculous cholecystitis by reducing exosomal CXCL16 secretion from macrophage and macrophage polarization. General significance: Our finding may provide a link between exosomes and neutrophils to serve as a potential therapeutic intervention in calculous cholecystitis.

Indexed as

Butyrate acidCalculous cholecystitisExosomal CXCL16Macrophage polarizationNeutrophil extracellular trapsformationNeutrophils migration

Identifiers

PMID38322881
PMCPMC10844290

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.