Evidence map›Paper›PMID 19286998›Full record

ArticleBlood2009

Targeted deletion of tumor suppressor PTEN augments neutrophil function and enhances host defense in neutropenia-associated pneumonia.

Yitang Li, Yonghui Jia, Muriel Pichavant, Fabien Loison, Bara Sarraj, Anongnard Kasorn, Jian You, Bryanne E Robson, Dale T Umetsu, Joseph P Mizgerd and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 56 citations in OpenAlex.

  1. Neutrophil death-more than meets the eye.Experimental hematology · 2025
    Review
  2. Article
  3. Article
  4. mSignal transduction and targeted therapy · 2022
    Article
  5. Article
  6. Review
  7. The Role of PTEN in Innate and Adaptive Immunity.Cold Spring Harbor perspectives in medicine · 2019
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. PTEN Inhibition in Human Disease Therapy.Molecules (Basel, Switzerland) · 2018
    Review
  14. Review
  15. Review
  16. Article
  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

12 authors at 4 institutions in 1 country.

Yitang LiDepartment of Pathology, Harvard Medical School, Dana-Farber/Harvard Cancer Center, Children's Hospital Boston, MA, USA.
Yonghui Jia
Muriel Pichavant
Fabien Loison
Bara Sarraj
Anongnard Kasorn
Jian You
Bryanne E Robson
Dale T Umetsu
Joseph P Mizgerd
Keqiang Ye
Hongbo R Luo
Dana-Farber/Harvard Cancer Center · USHarvard University · USBoston Children's Hospital · USEmory University · US

Funding

TRANSFUSION BIOLOGY AND MEDICINET32HL066987 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI JOHN P MANIS · 2001 to 2026
$10.2M
Molecular basis of neutrophil spontaneous deathR01HL085100 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI LUO, HONGBO R · 2007 to 2010
$2.0M
Signal transduction in neutrophil chemotaxisR01GM076084 · NIGMS · BOSTON CHILDREN'S HOSPITAL · PI LUO, HONGBO R · 2006 to 2010
$1.5M
NHLBI NIH HHS HL066987NHLBI NIH HHS HL085100NHLBI NIH HHS R01 HL085100NHLBI NIH HHS T32 HL066987NIGMS NIH HHS GM076084NIGMS NIH HHS R01 GM076084
6 · The paper itself

Abstract

Neutropenia and related infections are the most important dose-limiting toxicities in anticancer chemotherapy and radiotherapy. In this study, we explored a new strategy for augmenting host defense in neutropenia-related pneumonia. Phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P(3)) signaling in neutrophils was elevated by depleting PTEN, a phosphatidylinositol 3'-phosphatase that hydrolyzes PtdIns(3,4,5)P(3). In myeloid-specific PTEN knockout mice, significantly more neutrophils were recruited to the inflamed lungs during neutropenia-associated pneumonia. Using an adoptive transfer technique, we demonstrated that this enhancement could be caused directly by PTEN depletion in neutrophils. In addition, disruption of PTEN increased the recruitment of macrophages and elevated proinflammatory cytokines/chemokine levels in the inflamed lungs, which could also be responsible for the enhanced neutrophil recruitment. Depleting PTEN also significantly delayed apoptosis and enhanced the bacteria-killing capability of the recruited neutrophils. Finally, we provide direct evidence that enhancement of neutrophil function by elevating PtdIns(3,4,5)P(3) signaling can alleviate pneumonia-associated lung damage and decrease pneumonia-elicited mortality. Collectively, these results not only provide insight into the mechanism of action of PTEN and PtdIns(3,4,5)P(3) signaling pathway in modulating neutrophil function during lung infection and inflammation, but they also establish PTEN and related pathways as potential therapeutic targets for treating neutropenia-associated pneumonia.

Indexed as

AnimalsEscherichia coli InfectionsGene DeletionGene TargetingImmunity, InnateInflammationMiceMice, KnockoutNeutropeniaNeutrophil ActivationNeutrophilsPneumonia, BacterialPTEN PhosphohydrolaseSurvival AnalysisUp-RegulationPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID19286998
PMCPMC2686143
OpenAlexW2120549809

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.