Evidence map›Paper›PMID 25254554›Full record

ArticlePLoS pathogens2014

Hematopoietic but not endothelial cell MyD88 contributes to host defense during gram-negative pneumonia derived sepsis.

Miriam H P van Lieshout, Adam A Anas, Sandrine Florquin, Baidong Hou, Cornelis van't Veer, Alex F de Vos, Tom van der Poll

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  7. Hypoxia-Inducible Factor-1Mediators of inflammation · 2021
    Article
  8. Article
  9. Review
  10. Limited role of kininogen in the host response during gram-negative pneumonia-derived sepsis.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  11. Article
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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

7 authors at 3 institutions in 2 countries.

Miriam H P van LieshoutCenter of Infection and Immunity Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Center of Experimental and Molecular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
Adam A AnasCenter of Infection and Immunity Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Center of Experimental and Molecular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
Sandrine FlorquinDepartment of Pathology, Academic Medical Center, Amsterdam, the Netherlands.
Baidong HouKey Laboratory of Infection and Immunity, Institute of Biophysics, Chaoyang District, Beijing, China.
Cornelis van't VeerCenter of Infection and Immunity Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Center of Experimental and Molecular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
Alex F de VosCenter of Infection and Immunity Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Center of Experimental and Molecular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
Tom van der PollCenter of Infection and Immunity Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Center of Experimental and Molecular Medicine, Academic Medical Center, Amsterdam, the Netherlands; Division of Infectious Diseases, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Academic Medical Center · NLAmsterdam University of the Arts · NLInstitute of Biophysics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Klebsiella pneumoniae is an important cause of sepsis. The common Toll-like receptor adapter myeloid differentiation primary response gene (MyD)88 is crucial for host defense against Klebsiella. Here we investigated the role of MyD88 in myeloid and endothelial cells during Klebsiella pneumosepsis. Mice deficient for MyD88 in myeloid (LysM-Myd88(-/-)) and myeloid plus endothelial (Tie2-Myd88(-/-)) cells showed enhanced lethality and bacterial growth. Tie2-Myd88(-/-) mice reconstituted with control bone marrow, representing mice with a selective MyD88 deficiency in endothelial cells, showed an unremarkable antibacterial defense. Myeloid or endothelial cell MyD88 deficiency did not impact on lung pathology or distant organ injury during late stage sepsis, while LysM-Myd88(-/-) mice demonstrated a strongly attenuated inflammatory response in the airways early after infection. These data suggest that myeloid but not endothelial MyD88 is important for host defense during gram-negative pneumonia derived sepsis.

Indexed as

AnimalsBlotting, WesternBone Marrow TransplantationCells, CulturedCytokinesEndothelium, VascularFemaleHost-Pathogen InteractionsImmunity, InnateInflammationKlebsiella InfectionsKlebsiella pneumoniaeLungMaleMiceMice, Inbred C57BLCytokinesMyd88 protein, mouseMyeloid Differentiation Factor 88RNA, Messenger

Identifiers

PMID25254554
PMCPMC4177915
OpenAlexW2066003389

What OpenQuestion holds

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LicenceCC BY
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.