Evidence map›Paper›PMID 26994069›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2016

Monophosphoryl lipid A-induced pro-inflammatory cytokine expression does not require CD14 in primary human dendritic cells.

Sonja T H M Kolanowski, Suzanne N Lissenberg-Thunnissen, Diba Emal, S Marieke van Ham, Anja Ten Brinke

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Sonja T H M KolanowskiDivision Research and Landsteiner Laboratory, Sanquin Blood Supply, Department of Immunopathology, Academic Medical Center, University of Amsterdam, P.O. Box 9190, 1006 AD, Amsterdam, The Netherlands.
Suzanne N Lissenberg-ThunnissenDivision Research and Landsteiner Laboratory, Sanquin Blood Supply, Department of Immunopathology, Academic Medical Center, University of Amsterdam, P.O. Box 9190, 1006 AD, Amsterdam, The Netherlands.
Diba EmalDivision Research and Landsteiner Laboratory, Sanquin Blood Supply, Department of Immunopathology, Academic Medical Center, University of Amsterdam, P.O. Box 9190, 1006 AD, Amsterdam, The Netherlands.
S Marieke van HamDivision Research and Landsteiner Laboratory, Sanquin Blood Supply, Department of Immunopathology, Academic Medical Center, University of Amsterdam, P.O. Box 9190, 1006 AD, Amsterdam, The Netherlands.
Anja Ten BrinkeDivision Research and Landsteiner Laboratory, Sanquin Blood Supply, Department of Immunopathology, Academic Medical Center, University of Amsterdam, P.O. Box 9190, 1006 AD, Amsterdam, The Netherlands. a.tenbrinke@sanquin.nl.
Academic Medical Center · NLUniversity of Amsterdam · NLSanquin · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo elucidate if TLR4-mediated MyD88 and TRIF signalling by the clinically applicable Lipopolysaccharide (LPS)-derivative monophosphoryl lipid A (MPLA) in primary human dendritic cells requires LPS cofactors LPS-binding protein (LBP) and CD14.

methodsCytokine production by monocyte-derived DCs stimulated with MPLA or LPS was determined using ELISA. To investigate involvement of CD14 for action of LPS or MPLA, CD14 was inhibited using blocking antibodies or down-modulated using specific siRNA. To assess involvement of LBP monocyte-derived DCs were stimulated in serum-free culture medium in absence or presence of purified LBP.

resultsLBP and CD14 are not required for and do not enhance the capacity of MPLA to induce MyD88- and TRIF-dependent pro-inflammatory IL-6 and TNF-α. Interestingly, although CD14 is required for TRIF-dependent downstream events in mice, we show that in human CD14 is redundant for MPLA-induced TRIF-dependent chemokine production.

conclusionsThese findings provide novel insight in the modes of action of MPLA in human and show that, compared to LPS, MyD88 and TRIF signalling in dendritic cells by MPLA is not mediated nor amplified by TLR4 cofactors. This gives insight why MPLA induces immune activation without provoking toxicity in human and clarifies why MPLA can be used as activating compound for clinically applicable immuno-activatory cellular products grown in serum-free regimens.

Indexed as

Acute-Phase ProteinsAdaptor Proteins, Vesicular TransportCarrier ProteinsCells, CulturedCytokinesDendritic CellsDown-RegulationHumansLipid ALipopolysaccharide-Binding ProteinLipopolysaccharide ReceptorsLipopolysaccharidesMembrane GlycoproteinsMyeloid Differentiation Factor 88RNA, Small InterferingSignal TransductionAcute-Phase ProteinsAdaptor Proteins, Vesicular TransportCarrier ProteinsCytokinesLipid ALipopolysaccharide-Binding ProteinLipopolysaccharide ReceptorsLipopolysaccharidesMembrane Glycoproteinsmonophosphoryl lipid AMYD88 protein, humanMyeloid Differentiation Factor 88RNA, Small InterferingTICAM1 protein, humanAdjuvantsLBPMyD88TLR4Vaccine

Identifiers

PMID26994069
OpenAlexW2317162137

What OpenQuestion holds

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Registered trials

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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.