Evidence map›Paper›PMID 38323035›Full record

ReviewFrontiers in medicine2024

Exploring the role of IL-1β in inflammatory bowel disease pathogenesis.

Ioanna Aggeletopoulou, Maria Kalafateli, Efthymios P Tsounis, Christos Triantos

Abstract readReview
In one paragraph

Review in Frontiers in medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 3 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

68 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Effect ofFrontiers in pharmacology · 2025
    Pooled it
  4. Article
  5. Article
  6. Article
  7. Heterogeneous CRISPR/Cas9 Editing ofInternational journal of molecular sciences · 2026
    Article
  8. Review
  9. Article
  10. A Review on the Molecular Dynamics of EnterotypeInternational journal of molecular sciences · 2026
    Review
  11. Article
  12. Self-Assembly of Anti-Inflammatory Peptide Amphiphiles for Mucosal Health.Chembiochem : a European journal of chemical biology · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

8 more citing papers are in PubMed but not listed here.

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.

Ioanna AggeletopoulouDivision of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras, Greece.
Maria KalafateliDepartment of Gastroenterology, General Hospital of Patras, Patras, Greece.
Efthymios P TsounisDivision of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras, Greece.
Christos TriantosDivision of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras, Greece.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 1β (IL-1β) is a significant mediator of inflammation and tissue damage in IBD. The balance between IL-1β and its endogenous inhibitor-IL-1Ra-, plays a critical role in both initiation and regulation of inflammation. However, the precise role of IL-1β as a causative factor in IBD or simply a consequence of inflammation remains unclear. This review summarizes current knowledge on the molecular and cellular characteristics of IL-1β, describes the existing evidence on the role of this cytokine as a modulator of intestinal homeostasis and an activator of inflammatory responses, and also discusses the role of microRNAs in the regulation of IL-1β-related inflammatory responses in IBD. Current evidence indicates that IL-1β is involved in several aspects during IBD as it greatly contributes to the induction of pro-inflammatory responses through the recruitment and activation of immune cells to the gut mucosa. In parallel, IL-1β is involved in the intestinal barrier disruption and modulates the differentiation and function of T helper (Th) cells by activating the Th17 cell differentiation, known to be involved in the pathogenesis of IBD. Dysbiosis in the gut can also stimulate immune cells to release IL-1β, which, in turn, promotes inflammation. Lastly, increasing evidence pinpoints the central role of miRNAs involvement in IL-1β-related signaling during IBD, particularly in the maintenance of homeostasis within the intestinal epithelium. In conclusion, given the crucial role of IL-1β in the promotion of inflammation and immune responses in IBD, the targeting of this cytokine or its receptors represents a promising therapeutic approach. Further research into the IL-1β-associated post-transcriptional modifications may elucidate the intricate role of this cytokine in immunomodulation.

Indexed as

dysbiosisIL-1Rinflammasomeinflammatory bowel diseaseinterleukin 1βintestinal inflammationmiRNAs

Identifiers

PMID38323035
PMCPMC10845338

What OpenQuestion holds

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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.