Evidence map›Paper›PMID 23018458›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Insulin modulates the inflammatory granulocyte response to streptococci via phosphatidylinositol 3-kinase.

Sybille Kenzel, Miriam Mergen, Julius von Süßkind-Schwendi, Julia Wennekamp, Sachin D Deshmukh, Monika Haeffner, Antigoni Triantafyllopoulou, Sebastian Fuchs, Susan Farmand, Sandra Santos-Sierra and 4 more

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Vitamin D deficiency enhances insulin resistance by promoting inflammation in type 2 diabetes.International journal of clinical and experimental pathology · 2019
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Preserved effector functions of human ORAI1- and STIM1-deficient neutrophils.The Journal of allergy and clinical immunology · 2016
    Article
  9. Review
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

14 authors at 4 institutions in 2 countries.

Sybille KenzelCenter for Pediatric and Adolescent Medicine, University of Freiburg, 79106 Freiburg, Germany.
Miriam Mergen
Julius von Süßkind-Schwendi
Julia Wennekamp
Sachin D Deshmukh
Monika Haeffner
Antigoni Triantafyllopoulou
Sebastian Fuchs
Susan Farmand
Sandra Santos-Sierra
Jochen Seufert
Timo K van den Berg
Taco W Kuijpers
Philipp Henneke
University Medical Center Freiburg · DEUniversity of Freiburg · DESanquin · NLUniversity of Amsterdam · NL

Funding

Group B. Streptococci and Toll-like ReceptorsR01AI052455 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GOLENBOCK, DOUGLAS T · 2002 to 2012
$4.2M
NIAID NIH HHS R01 AI052455NIAID NIH HHS R0I AI052455-06A1
6 · The paper itself

Abstract

Group B streptococci (GBS; Streptococcus agalactiae) are a major cause of invasive infections in newborn infants and in patients with type 2 diabetes. Both patient groups exhibit peripheral insulin resistance and alterations in polymorphonuclear leukocyte (PML) function. In this investigation, we studied the PML response repertoire to GBS with a focus on TLR signaling and the modulation of this response by insulin in mice and humans. We found that GBS-induced, MyD88-dependent chemokine formation of PML was specifically downmodulated by insulin via insulin receptor-mediated induction of PI3K. PI3K inhibited transcription of chemokine genes on the level of NF-κB activation and binding. Insulin specifically modulated the chemokine response of PML to whole bacteria, but affected neither activation by purified TLR agonists nor antimicrobial properties, such as migration, phagocytosis, bacterial killing, and formation of reactive oxygen species. The targeted modulation of bacteria-induced chemokine formation by insulin via PI3K may form a basis for the development of novel targets of adjunctive sepsis therapy.

Indexed as

AdultAnimalsGranulocytesHumansInfant, NewbornInflammationInsulinInsulin ResistanceMiceMice, Inbred C57BLMice, KnockoutPhosphatidylinositol 3-KinaseStreptococcus agalactiaeInsulinPhosphatidylinositol 3-Kinase

Identifiers

PMID23018458
PMCPMC5417076
OpenAlexW2162476947

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.