Evidence map›Paper›PMID 31708927›Full record

ArticleFrontiers in immunology2019

Leukocyte-Released Mediators in Response to Both Bacterial and Fungal Infections Trigger IFN Pathways, Independent of IL-1 and TNF-α, in Endothelial Cells.

Kieu T T Le, Xiaojing Chu, Martin Jaeger, Josée A Plantinga, Vasiliki Matzaraki, Sebo Withoff, Leo A B Joosten, Mihai G Netea, Cisca Wijmenga, Yang Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. 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
1.3field-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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  5. Review
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  11. Observational
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  13. The CompoundPharmaceutics · 2022
    Article
  14. Review
  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

12 authors at 4 institutions in 2 countries.

Kieu T T LeDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Xiaojing ChuDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Martin JaegerDepartment of Internal Medicine and Radboud Centre for Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, Netherlands.
Josée A PlantingaDepartment of Pathology and Medical Biology, Medical Biology Section, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Vasiliki MatzarakiDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Sebo WithoffDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Leo A B JoostenDepartment of Internal Medicine and Radboud Centre for Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, Netherlands.
Mihai G NeteaDepartment of Internal Medicine and Radboud Centre for Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, Netherlands.
Cisca WijmengaDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Yang LiDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Jill MoserDepartment of Pathology and Medical Biology, Medical Biology Section, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Vinod KumarDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
University of Groningen · NLUniversity Medical Center Groningen · NLRadboud University Medical Center · NLRadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In sepsis, dysregulated immune responses to infections cause damage to the host. Previous studies have attempted to capture pathogen-induced leukocyte responses. However, the impact of mediators released after pathogen-leukocyte interaction on endothelial cells, and how endothelial cell responses vary depending on the pathogen-type is lacking. Here, we comprehensively characterized the transcriptomic responses of human leukocytes and endothelial cells to Gram negative-bacteria, Gram positive-bacteria, and fungi. We showed that whole pathogen lysates induced strong activation of leukocytes but not endothelial cells. Interestingly, the common response of leukocytes to various pathogens converges on endothelial activation. By exposing endothelial cells to leukocyte-released mediators, we observed a strong activation of endothelial cells at both transcription and protein levels. By adding IL-1RA and TNF-α antibody in leukocyte-released mediators before exposing to endothelial cells, we identified specific roles for IL-1 and TNF-α in driving the most, but not all, endothelial activation. We also showed for the first time, activation of interferon response by endothelial cells in response to leukocyte-released mediators, independently from IL-1 and TNF-α pathways. Our study therefore, not only provides pathogen-dependent transcriptional changes in leukocytes and endothelial cells during infections, but also reveals a role for IFN, together with IL1 and TNFα signaling, in mediating leukocyte-endothelial interaction in infections.

Indexed as

Bacterial InfectionsCell CommunicationCells, CulturedEndothelial CellsHumansInterferonsInterleukin-1LeukocytesMycosesSignal TransductionTumor Necrosis Factor-alphaInterferonsInterleukin-1Tumor Necrosis Factor-alphabacterial infectionendothelial transcriptomesfungal infectioninterferon pathwaysleukocyte-endothelial interactionleukocyte transcriptomessepsis

Identifiers

PMID31708927
PMCPMC6824321
OpenAlexW2981361732

What OpenQuestion holds

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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.