Evidence map›Paper›PMID 36240261›Full record

ArticlePLoS pathogens2022

TLR2 axis on peripheral blood mononuclear cells regulates inflammatory responses to non-infectious immature dengue virus particles.

José Alberto Aguilar Briseño, Lennon Ramos Pereira, Marleen van der Laan, Mindaugas Pauzuolis, Bram M Ter Ellen, Vinit Upasani, Jill Moser, Luís Carlos de Souza Ferreira, Jolanda M Smit, Izabela A Rodenhuis-Zybert

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 13% 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, 2 syntheses or guidelines pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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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

10 authors at 2 institutions in 3 countries.

José Alberto Aguilar BriseñoDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.ORCID 0000-0002-7293-4027
Lennon Ramos PereiraVaccine Development Laboratory, Microbiology Department, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Marleen van der LaanDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
Mindaugas PauzuolisDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
Bram M Ter EllenDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
Vinit UpasaniDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
Jill MoserDepartments of Critical Care, Pathology & Medical Biology, Medical Biology section, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Luís Carlos de Souza FerreiraVaccine Development Laboratory, Microbiology Department, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Jolanda M SmitDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
Izabela A Rodenhuis-ZybertDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.ORCID 0000-0002-7820-8624
University Medical Center Groningen · NLUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe dengue virus (DENV) infection is characterized by exacerbated inflammatory responses that lead to endothelial dysfunction and plasma leakage. We have recently demonstrated that Toll-like receptor 2 (TLR2) on blood monocytes senses DENV infection leading to endothelial activation. Here, we report that non-infectious immature DENV particles, which are released in large numbers by DENV-infected cells, drive endothelial activation via the TLR2 axis. We show that fully immature DENV particles induce a rapid, within 6 hours post-infection, inflammatory response in PBMCs. Furthermore, pharmacological blocking of TLR2/TLR6/CD14 and/or NF-kB prior to exposure of PBMCs to immature DENV reduces the initial production of inter alia TNF-α and IL-1β by monocytes and prevents endothelial activation. However, prolonged TLR2 block induces TNF-α production and leads to exacerbated endothelial activation, indicating that TLR2-mediated responses play an important role not only in the initiation but also the resolution of inflammation. Altogether, these data indicate that the maturation status of the virus has the potential to influence the kinetics and extent of inflammatory responses during DENV infection.

Indexed as

DengueDengue VirusHumansInflammationLeukocytes, MononuclearNF-kappa BToll-Like Receptor 2Toll-Like Receptor 6Tumor Necrosis Factor-alphaVirionNF-kappa BTLR2 protein, humanToll-Like Receptor 2Toll-Like Receptor 6Tumor Necrosis Factor-alpha

Identifiers

PMID36240261
PMCPMC9605289
OpenAlexW4306247963

What OpenQuestion holds

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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.