Evidence map›Paper›PMID 27444882›Full record

ArticleScientific reports2016

Differential in vivo activation of monocyte subsets during low-grade inflammation through experimental endotoxemia in humans.

B Thaler, P J Hohensinner, K A Krychtiuk, P Matzneller, L Koller, M Brekalo, G Maurer, K Huber, M Zeitlinger, B Jilma and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
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  5. Circulating Fibrocytes: Cellular Mediators of Tissue Fibrosis.International journal of molecular sciences · 2026
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  16. The role of monocytes in thrombotic diseases: a review.Frontiers in cardiovascular medicine · 2023
    Review
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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

12 authors at 3 institutions in 1 country.

B ThalerDepartment of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
P J HohensinnerDepartment of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
K A KrychtiukDepartment of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
P MatznellerDepartment of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
L KollerDepartment of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
M BrekaloDepartment of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
G MaurerDepartment of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
K Huber3rd Medical Department for Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria.
M ZeitlingerDepartment of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
B JilmaDepartment of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
J WojtaDepartment of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
W S SpeidlDepartment of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATLudwig Boltzmann Cluster for Cardiovascular Research · ATWilhelminen Hospital · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human monocytes are a heterogeneous cell population, which can be divided into a classical (CD14++CD16-), a non-classical (CD14+CD16+), and an intermediate (CD14++CD16+) subset. We hypothesized that low-grade inflammation may differentially affect monocyte subsets. We used a human lipopolysaccharide (LPS) infusion model to mimic low-grade inflammation to identify, which monocyte subsets are preferentially activated under these conditions. Monocyte subsets were identified by staining for CD14 and CD16, activation status of monocytes was analyzed by staining for CD11b and a novel in situ mRNA hybridization approach to detect IL-6 and IL-8 specific mRNA at the single-cell level by flow cytometry. After LPS challenge, cell numbers of monocyte subsets dropped after 2 h with cell numbers recovering after 6 h. Distribution of monocyte subsets was skewed dramatically towards the intermediate subset after 24 h. Furthermore, intermediate monocytes displayed the largest increase of CD11b expression after 2 h. Finally, IL-6 and IL-8 mRNA levels increased in intermediate and non-classical monocytes after 6 h whereas these mRNA levels in classical monocytes changed only marginally. In conclusion, our data indicates that the main responding subset of monocytes to standardized low-grade inflammation induced by LPS in humans is the CD14++CD16+ intermediate subset followed by the CD14+CD16+ non-classical monocyte subset. Circulating classical monocytes showed comparably less reaction to LPS challenge in vivo.

Indexed as

Cell CountEndotoxemiaHumansInflammationInterleukin-6Interleukin-8Lipopolysaccharide ReceptorsLipopolysaccharidesMonocytesReceptors, IgGRNA, MessengerInterleukin-6Interleukin-8Lipopolysaccharide ReceptorsLipopolysaccharidesReceptors, IgGRNA, Messenger

Identifiers

PMID27444882
PMCPMC4957086
OpenAlexW2476067827

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.