Evidence map›Paper›PMID 19689736›Full record

ArticleImmunology2009

A central role for monocytes in Toll-like receptor-mediated activation of the vasculature.

Jon R Ward, Sheila E Francis, Luke Marsden, Tesha Suddason, Graham M Lord, Steven K Dower, David C Crossman, Ian Sabroe

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

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  14. Diesel exhaust particles override natural injury-limiting pathways in the lung.American journal of physiology. Lung cellular and molecular physiology · 2010
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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

8 authors at 2 institutions in 1 country.

Jon R WardCardiovascular Research Unit, School of Medicine and Biomedical Sciences, The University of Sheffield, Sheffield, UK.
Sheila E Francis
Luke Marsden
Tesha Suddason
Graham M Lord
Steven K Dower
David C Crossman
Ian Sabroe
King's College London · GBUniversity of Sheffield · GB

Funding

British Heart Foundation FS/06/004Medical Research Council G0802068Medical Research Council G116/170
6 · The paper itself

Abstract

There is increasing evidence that activation of inflammatory responses in a variety of tissues is mediated co-operatively by the actions of more than one cell type. In particular, the monocyte has been implicated as a potentially important cell in the initiation of inflammatory responses to Toll-like receptor (TLR)-activating signals. To determine the potential for monocyte-regulated activation of tissue cells to underpin inflammatory responses in the vasculature, we established cocultures of primary human endothelial cells and monocytes and dissected the inflammatory responses of these systems following activation with TLR agonists. We observed that effective activation of inflammatory responses required bidirectional signalling between the monocyte and the tissue cell. Activation of cocultures was dependent on interleukin-1 (IL-1). Although monocyte-mediated IL-1beta production was crucial to the activation of cocultures, TLR specificity to these responses was also provided by the endothelial cells, which served to regulate the signalling of the monocytes. TLR4-induced IL-1beta production by monocytes was increased by TLR4-dependent endothelial activation in coculture, and was associated with increased monocyte CD14 expression. Activation of this inflammatory network also supported the potential for downstream monocyte-dependent T helper type 17 activation. These data define co-operative networks regulating inflammatory responses to TLR agonists, identify points amenable to targeting for the amelioration of vascular inflammation, and offer the potential to modify atherosclerotic plaque instability after a severe infection.

Indexed as

Cell CommunicationCell SurvivalCoculture TechniquesCytokinesDose-Response Relationship, ImmunologicEndothelial CellsEndothelium, VascularHumansInflammationInterleukin-1Lipopolysaccharide ReceptorsLipopolysaccharidesMonocytesSignal TransductionT-Lymphocytes, Helper-InducerToll-Like Receptor 2CytokinesInterleukin-1Lipopolysaccharide ReceptorsLipopolysaccharidesTLR2 protein, humanToll-Like Receptor 2Toll-Like Receptors

Identifiers

PMID19689736
PMCPMC2747139
OpenAlexW2100417658

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.