Evidence map›Paper›PMID 23869087›Full record

ArticleBlood2013

Staphylococcus aureus recognition by hematopoietic stem and progenitor cells via TLR2/MyD88/PGE2 stimulates granulopoiesis in wounds.

Jennifer L Granick, Patrick C Falahee, Delsheen Dahmubed, Dori L Borjesson, Lloyd S Miller, Scott I Simon

Abstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Neutrophils in Physiology and Pathology.Annual review of pathology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Upregulation of PD-L1 Expression by Prostaglandin EFrontiers in veterinary science · 2020
    Article
  15. Article
  16. Observational
  17. Article
  18. Article
  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

6 authors at 3 institutions in 1 country.

Jennifer L GranickDepartment of Veterinary Clinical Sciences, University of Minnesota College of Veterinary Medicine, St. Paul, MN;
Patrick C Falahee
Delsheen Dahmubed
Dori L Borjesson
Lloyd S Miller
Scott I Simon
University of California, Davis · USJohns Hopkins University · USUniversity of Minnesota · US

Funding

Animal Models of Infectious Diseases Training ProgramT32AI060555 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI MCSORLEY, STEPHEN J · 2004 to 2025
$3.3M
Innate Immune Response to Staphylococcus aureus in SkinR01AI078910 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MILLER, LLOYD S · 2009 to 2013
$1.7M
NIAID NIH HHS R01 AI078910NIAID NIH HHS T32 AI060555
6 · The paper itself

Abstract

During bacterial infection, hematopoietic stem and progenitor cells (HSPCs) differentiate into polymorphonuclear leukocytes (PMNs) in the bone marrow. We reported that HSPCs recruited to Staphylococcus aureus-infected skin wounds in mice undergo granulopoiesis, whereas other authors have demonstrated their differentiation in vitro after Toll-like receptor 2 (TLR2)/MyD88 stimulation. Here, we examined this pathway in HSPC trafficking and granulopoiesis within S aureus-infected wounds. Lineage- HSPCs from TLR2- or MyD88-deficient mice injected into infected wounds of wild-type (WT) mice exhibited impaired granulopoiesis. However, HSPCs from WT mice produced similar numbers of PMNs whether transferred into wounds of TLR2-, MyD88-deficient, or WT mice. Prostaglandin E2 (PGE2), which stimulates HSPC survival and proliferation, was produced by HSPCs after TLR2 stimulation, suggesting that TLR2/MyD88 activation promotes granulopoiesis in part by production and autocrine activity of PGE2. Pretreatment of TLR2- or MyD88-deficient HSPCs with PGE2 rescued granulocytic differentiation in vivo. Finally, we demonstrate that bone marrow-derived lin-/Sca-1+/c-kit+ cells produced PGE2 and underwent granulopoiesis after TLR2 stimulation. lin-/Sca-1+/c-kit+ cells deficient in TLR2 or MyD88 produced PMNs after PGE2 treatment when transferred into uninfected wounds. We conclude that granulopoiesis in S aureus-infected wounds is induced by TLR2/MyD88 activation of HSPCs through a mechanism that involves autocrine production and activity of PGE2.

Indexed as

LeukopoiesisAnimalsBone MarrowCell CountCell DifferentiationCell ProliferationCell SeparationDinoprostoneFemaleGranulocytesHematopoietic Stem CellsImmunity, InnateMaleMiceMice, Inbred C57BLMice, KnockoutDinoprostoneMyeloid Differentiation Factor 88Toll-Like Receptor 2

Identifiers

PMID23869087
PMCPMC3765058
OpenAlexW2090885069

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.