Evidence map›Paper›PMID 29263351›Full record

ArticleScientific reports2017

Interleukin-33 modulates inflammation in endometriosis.

Jessica E Miller, Stephany P Monsanto, Soo Hyun Ahn, Kasra Khalaj, Asgerally T Fazleabas, Steven L Young, Bruce A Lessey, Madhuri Koti, Chandrakant Tayade

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.6field-weighted citation impact, top 3% of its field
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

58 citing papers in PubMed, 127 citations in OpenAlex.

  1. Review
  2. Article
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  7. Review
  8. The role of IL-33/ST2 signaling in female reproductive diseases.Frontiers in cell and developmental biology · 2026
    Review
  9. Article
  10. Review
  11. Review
  12. Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025
    Review
  13. Article
  14. Article
  15. Modelling Endometriosis Using In Vitro and In Vivo Systems.International journal of molecular sciences · 2025
    Review
  16. Article
  17. Article
  18. Review
  19. Review
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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

9 authors at 4 institutions in 2 countries.

Jessica E MillerDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, K7L 3N6, Canada.
Stephany P MonsantoDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, K7L 3N6, Canada.
Soo Hyun AhnDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, K7L 3N6, Canada.
Kasra KhalajDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, K7L 3N6, Canada.
Asgerally T FazleabasDepartment of Obstetrics, Gynecology and Reproductive Biology, Michigan State University College of Human Medicine, Grand Rapids, MI, 49503, USA.
Steven L YoungDepartment of Obstetrics and Gynecology, University of North Carolina, Chapel Hill, North Carolina, NC, 27514, USA.
Bruce A LesseyDepartment of Obstetrics and Gynecology, Greenville Health Systems, Greenville, South Carolina, SC, 29605, USA.
Madhuri KotiDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, K7L 3N6, Canada.
Chandrakant TayadeDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, K7L 3N6, Canada. tayadec@queensu.ca.
Queen's University · CAGrand Rapids Community College · USPrisma Health · USUniversity of North Carolina at Chapel Hill · US

Funding

Progesterone Action in the Endometrium of Women with EndometriosisR01HD067721 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI YOUNG, STEVEN L · 2011 to 2015
$3.1M
CIHR
6 · The paper itself

Abstract

Endometriosis is a debilitating condition that is categorized by the abnormal growth of endometrial tissue outside the uterus. Although the pathogenesis of this disease remains unknown, it is well established that endometriosis patients exhibit immune dysfunction. Interleukin (IL)-33 is a danger signal that is a critical regulator of chronic inflammation. Although plasma and peritoneal fluid levels of IL-33 have been associated with deep infiltrating endometriosis, its contribution to the disease pathophysiology is unknown. We investigated the role of IL-33 in the pathology of endometriosis using patient samples, cell lines and a syngeneic mouse model. We found that endometriotic lesions produce significantly higher levels of IL-33 compared to the endometrium of healthy, fertile controls. In vitro stimulation of endometrial epithelial, endothelial and endometriotic epithelial cells with IL-33 led to the production of pro-inflammatory and angiogenic cytokines. In a syngeneic mouse model of endometriosis, IL-33 injections caused systemic inflammation, which manifested as an increase in plasma pro-inflammatory cytokines compared to control mice. Furthermore, endometriotic lesions from IL-33 treated mice were highly vascularized and exhibited increased proliferation. Collectively, we provide convincing evidence that IL-33 perpetuates inflammation, angiogenesis and lesion proliferation, which are critical events in the lesion survival and progression of endometriosis.

Indexed as

AnimalsAscitic FluidCell LineCell Line, TumorCytokinesDisease Models, AnimalEndometriosisEndometriumFemaleHumansHuman Umbilical Vein Endothelial CellsInflammationInterleukin-33Interleukin-8MiceMice, Inbred C57BLCytokinesIL33 protein, humanInterleukin-33Interleukin-8

Identifiers

PMID29263351
PMCPMC5738435
OpenAlexW2771136649

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.