Evidence map›Paper›PMID 29315356›Full record

ArticleBiology of reproduction2018

Interleukin 22 prevents lipopolysaccharide- induced preterm labor in mice.

Svetlana Dambaeva, Sylvia Schneiderman, Mukesh K Jaiswal, Varkha Agrawal, Gajendra K Katara, Alice Gilman-Sachs, Emmet Hirsch, Kenneth D Beaman

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. A rare variant in theArchives of medical science : AMS · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Innate Lymphoid Cells at the Maternal-Fetal Interface in Human Pregnancy.International journal of biological sciences · 2020
    Review
  19. Article
  20. 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 at 2 institutions in 1 country.

Svetlana DambaevaDepartment of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Sylvia SchneidermanDepartment of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Mukesh K JaiswalDepartment of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Varkha AgrawalDepartment of Obstetrics and Gynecology, NorthShore University HealthSystem, Evanston, Illinois, USA.
Gajendra K KataraDepartment of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Alice Gilman-SachsDepartment of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Emmet HirschDepartment of Obstetrics and Gynecology, NorthShore University HealthSystem, Evanston, Illinois, USA.
Kenneth D BeamanDepartment of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
Rosalind Franklin University of Medicine and Science · USNorthShore University HealthSystem · US

Funding

Toll-like receptor signaling in the pathogenesis and prevention of prematurityR01HD056118 · NICHD · ENDEAVOR HEALTH CLINICAL OPERATIONS · PI HIRSCH, EMMET · 2008 to 2012
$1.8M
NICHD NIH HHS R01 HD056118
6 · The paper itself

Abstract

Preterm birth is widespread and causes 35% of all neonatal deaths. Infants who survive face potential long-term complications. A major contributing factor of preterm birth is infection. We investigated the role of interleukin 22 (IL22) as a potential clinically relevant cytokine during gestational infection. IL22 is an effector molecule secreted by immune cells. While the expression of IL22 was reported in normal nonpregnant endometrium and early pregnancy decidua, little is known about uterine IL22 expression during mid or late gestational stages of pregnancy. Since IL22 has been shown to be an essential mediator in epithelial regeneration and wound repair, we investigated the potential role of IL22 during defense against an inflammatory response at the maternal-fetal interface. We used a well-established model to study infection and infection-associated inflammation during preterm birth in the mouse. We have shown that IL22 is upregulated to respond to an intrauterine lipopolysaccharide administration and plays an important role in controlling the risk of inflammation-induced preterm birth. This paper proposes IL22 as a treatment method to combat infection and prevent preterm birth in susceptible patients.

Indexed as

AnimalsCaspasesFas Ligand ProteinFemaleInterleukin-22InterleukinsLipopolysaccharidesMiceObstetric Labor, PrematurePregnancyUp-RegulationUterusCaspasesFas Ligand ProteinInterleukin-22InterleukinsLipopolysaccharides

Identifiers

PMID29315356
PMCPMC6669419
OpenAlexW2782505428

What OpenQuestion holds

Textmetadata
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.