Evidence map›Paper›PMID 23902376›Full record

ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2014

EP4 and EP2 receptor activation of protein kinase A by prostaglandin E2 impairs macrophage phagocytosis of Clostridium sordellii.

Lisa M Rogers, Tennille Thelen, Krystle Fordyce, Emilie Bourdonnay, Casey Lewis, Han Yu, Junyong Zhang, Jingli Xie, Carlos H Serezani, Marc Peters-Golden and 1 more

Abstract read
In one paragraph

Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Upregulation ofEpigenetics · 2024
    Article
  2. SPMs exert anti-inflammatory and pro-resolving effects through positive allosteric modulation of the prostaglandin EP4 receptor.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
  5. Eicosanoid regulation of debris-stimulated metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  6. Article
  7. Decidual stromal cell-derived PGEAmerican journal of reproductive immunology (New York, N.Y. : 1989) · 2018
    Article
  8. Prostaglandin EPharmacology & therapeutics · 2018
    Review
  9. The prostaglandin EThe Journal of reproduction and development · 2018
    Article
  10. Prostaglandins DJournal of lipid research · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

11 authors at 5 institutions in 2 countries.

Lisa M RogersDivision of Infectious Diseases, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, MI, USA.
Tennille Thelen
Krystle Fordyce
Emilie Bourdonnay
Casey Lewis
Han Yu
Junyong Zhang
Jingli Xie
Carlos H Serezani
Marc Peters-Golden
David M Aronoff
Michigan Medicine · USJiaxing University · CNIndiana University – Purdue University Indianapolis · USUniversity of Michigan–Ann Arbor · USUniversity of Washington · US

Funding

Role of misoprostol in Clostridium sordellii endometritis in a rodent modelR01HD057176 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ARONOFF, DAVID M · 2008 to 2012
$1.6M
NICHD NIH HHS HD057176NICHD NIH HHS R01 HD057176
6 · The paper itself

Abstract

problemClostridium sordellii causes endometrial infections, but little is known regarding host defenses against this pathogen. METHOD OF STUDY: We tested the hypothesis that the immunoregulatory lipid prostaglandin (PG) E2 suppresses human macrophage clearance of C. sordellii through receptor-induced increases in intracellular cyclic adenosine monophosphate (cAMP). The THP-1 macrophage cell line was used to quantify C. sordellii phagocytosis.

resultsPGE2 increased cAMP levels, activated protein kinase A (PKA), and inhibited the class A scavenger receptor-dependent phagocytosis of C. sordellii. Activation of the EP2 and EP4 receptors increased intracellular cAMP and inhibited phagocytosis, with evidence favoring a more important role for EP4 over EP2. This was supported by EP receptor expression data and the use of pharmacological receptor antagonists. In addition, the PKA isoform RI appeared to be more important than RII in mediating the suppression of ingestion of C. sordellii.

conclusionThe endogenous lipid mediator PGE2 impairs human innate immune responses against C. sordellii.

Indexed as

Cell LineClostridium InfectionsCyclic AMPCyclic AMP-Dependent Protein KinasesDinoprostoneHumansImmune ToleranceImmunity, InnateMacrophagesParaclostridium sordelliiPhagocytosisProtein IsoformsReceptors, Prostaglandin E, EP2 SubtypeReceptors, Prostaglandin E, EP4 SubtypeCyclic AMPCyclic AMP-Dependent Protein KinasesDinoprostoneProtein IsoformsReceptors, Prostaglandin E, EP2 SubtypeReceptors, Prostaglandin E, EP4 SubtypeAbortionendometritisinnate immunityphagocytosispregnancytoxic shock syndrome

Identifiers

PMID23902376
PMCPMC3864121
OpenAlexW2091214448

What OpenQuestion holds

Textmetadata
LicenceTDM
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.