Evidence map›Paper›PMID 22768282›Full record

ArticlePloS one2012

Adherent human alveolar macrophages exhibit a transient pro-inflammatory profile that confounds responses to innate immune stimulation.

Gillian S Tomlinson, Helen Booth, Sarah J Petit, Elspeth Potton, Greg J Towers, Robert F Miller, Benjamin M Chain, Mahdad Noursadeghi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed, 64 citations in OpenAlex.

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  14. BiodiversemSphere · 2020
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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 1 institution in 1 country.

Gillian S TomlinsonInfection and Immunity, University College London, London, United Kingdom.
Helen Booth
Sarah J Petit
Elspeth Potton
Greg J Towers
Robert F Miller
Benjamin M Chain
Mahdad Noursadeghi
University College London · GB

Funding

Medical Research Council G0700569Medical Research Council G0801172Medical Research Council G0900950Medical Research Council G9721629Wellcome Trust 090940Wellcome Trust WT077161
6 · The paper itself

Abstract

Alveolar macrophages (AM) are thought to have a key role in the immunopathogenesis of respiratory diseases. We sought to test the hypothesis that human AM exhibit an anti-inflammatory bias by making genome-wide comparisons with monocyte derived macrophages (MDM). Adherent AM obtained by bronchoalveolar lavage of patients under investigation for haemoptysis, but found to have no respiratory pathology, were compared to MDM from healthy volunteers by whole genome transcriptional profiling before and after innate immune stimulation. We found that freshly isolated AM exhibited a marked pro-inflammatory transcriptional signature. High levels of basal pro-inflammatory gene expression gave the impression of attenuated responses to lipopolysaccharide (LPS) and the RNA analogue, poly IC, but in rested cells pro-inflammatory gene expression declined and transcriptional responsiveness to these stimuli was restored. In comparison to MDM, both freshly isolated and rested AM showed upregulation of MHC class II molecules. In most experimental paradigms ex vivo adherent AM are used immediately after isolation. Therefore, the confounding effects of their pro-inflammatory profile at baseline need careful consideration. Moreover, despite the prevailing view that AM have an anti-inflammatory bias, our data clearly show that they can adopt a striking pro-inflammatory phenotype, and may have greater capacity for presentation of exogenous antigens than MDM.

Indexed as

Antigen PresentationCell AdhesionCells, CulturedCell SeparationGene Expression ProfilingGenome, HumanHistocompatibility Antigens Class IIHumansImmunity, InnateInflammationLipopolysaccharidesMacrophages, AlveolarPhenotypeTime FactorsTranscription FactorsUp-RegulationHistocompatibility Antigens Class IILipopolysaccharidesTranscription Factors

Identifiers

PMID22768282
PMCPMC3386998
OpenAlexW1983316303

What OpenQuestion holds

Textmetadata
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.