Evidence map›Paper›PMID 23637950›Full record

ArticlePloS one2013

The response of human macrophages to β-glucans depends on the inflammatory milieu.

Cristina Municio, Yolanda Alvarez, Olimpio Montero, Etzel Hugo, Mario Rodríguez, Esther Domingo, Sara Alonso, Nieves Fernández, Mariano Sánchez Crespo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Saccharomyces cerevisiae β-glucan improves the response of trained macrophages to severe P. aeruginosa infections.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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  5. Review
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  7. The efficacy of metal nanocomposite (FeBMC veterinary research · 2022
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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

9 authors at 2 institutions in 1 country.

Cristina MunicioInstituto de Biología y Genética Molecular, CSIC, Valladolid, Spain.
Yolanda Alvarez
Olimpio Montero
Etzel Hugo
Mario Rodríguez
Esther Domingo
Sara Alonso
Nieves Fernández
Mariano Sánchez Crespo
Instituto de Biomedicina y Genética Molecular de Valladolid · ESUniversidad de Valladolid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundβ-glucans are fungal cell wall components that bind to the C-type lectin-like receptor dectin-1. Polymorphisms of dectin-1 gene are associated with susceptibility to invasive fungal infection and medically refractory ulcerative colitis. The purpose of this study has been addressing the response of human macrophages to β-glucans under different conditions mimicking the composition of the inflammatory milieu in view of the wide plasticity and large range of phenotypical changes showed by these cells, and the relevant role of dectin-1 in several pathophysiological conditions. PRINCIPAL

findingsSerum-differentiated macrophages stimulated with β-glucans showed a low production of TNFα and IL-1β, a high production of IL-6 and IL-23, and a delayed induction of cyclooxygenase-2 and PGE2 biosynthesis that resembled the responses elicited by crystals and those produced when phagosomal degradation of the phagocytic cargo increases ligand access to intracellular pattern recognition receptors. Priming with a low concentration of LPS produced a rapid induction of cyclooxygenase-2 and a synergistic release of PGE2. When the differentiation of the macrophages was carried out in the presence of M-CSF, an increased expression of dectin-1 B isoform was observed. In addition, this treatment made the cells capable to release arachidonic acid in response to β-glucan.

conclusionsThese results indicate that the macrophage response to fungal β-glucans is strongly influenced by cytokines and microbial-derived factors that are usual components of the inflammatory milieu. These responses can be sorted into three main patterns i) an elementary response dependent on phagosomal processing of pathogen-associated molecular patterns and/or receptor-independent, direct membrane binding linked to the immunoreceptor tyrosine-based activation motif-bearing transmembrane adaptor DNAX-activating protein 12, ii) a response primed by TLR4-dependent signals, and iii) a response dependent on M-CSF and dectin-1 B isoform expression that mainly signals through the dectin-1 B/spleen tyrosine kinase/cytosolic phospholipase A2 route.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsArachidonic Acidbeta-GlucansCyclooxygenase 2CytokinesDectin-1Dendritic CellsDinoprostoneEnzyme ActivationGene DeletionHumansInflammationLectins, C-TypeMacrophagesMiceAdaptor Proteins, Signal TransducingArachidonic Acidbeta-GlucansCyclooxygenase 2CytokinesDectin-1DinoprostoneLectins, C-TypeNF-kappa BZymosan

Identifiers

PMID23637950
PMCPMC3634770
OpenAlexW2040397671

What OpenQuestion holds

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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.