Evidence map›Paper›PMID 16907912›Full record

ArticleClinical and experimental immunology2006

Triggering receptor expressed on myeloid cells (TREM-1) is regulated post-transcriptionally and its ligand is present in the sera of some septic patients.

I Wong-Baeza, N González-Roldán, E Ferat-Osorio, N Esquivel-Callejas, R Aduna-Vicente, L Arriaga-Pizano, H Astudillo-de la Vega, M A Villasis-Keever, R Torres-González, I Estrada-García and 2 more

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

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  9. sTREM-1, sIL-2Rα, and IL-6, but not sCD163, might predict sepsis in polytrauma patients: a prospective cohort study.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2017
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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.

I Wong-BaezaUnidad de Investigación Médica en Inmunoquímica, Hospital de Especialidades, Mexico DF, Mexico.
N González-Roldán
E Ferat-Osorio
N Esquivel-Callejas
R Aduna-Vicente
L Arriaga-Pizano
H Astudillo-de la Vega
M A Villasis-Keever
R Torres-González
I Estrada-García
C López-Macías
A Isibasi
Hospital de Especialidades · MXInstituto Politécnico Nacional · MXCentro Medico Nacional Siglo XXI · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is necessary for survival, but it is also an important cause of human morbidity and mortality, as exemplified by sepsis. During inflammation, cells of the innate immune system are recruited and activated in response to infection, trauma or injury. These cells are activated through receptors, such as Toll-like receptors (TLRs), which recognize microbial ligands such as lipopolysaccharide (LPS). Triggering receptor expressed on myeloid cells (TREM)-1 amplifies the inflammatory response initiated by TLRs, and its expression on the surface of monocytes increases in the presence of TLR ligands. Here we have shown that in monocytes TREM-1 mRNA levels, measured by reverse transcription-polymerase chain reaction (RT-PCR), remained unchanged and TREM-1 protein levels, measured by flow cytometry, increased, indicating that LPS increases TREM-1 expression by a post-transcriptional mechanism. We also showed that TREM-1/Fc fusion protein decreased the ability of the sera of some patients with sepsis to activate monocytes, indicating that the TREM-1 ligand, whose identity is unknown, may be present in the sera of some of these patients. We describe a mechanism for the regulation of TREM-1 expression on monocytes and the possible presence of its ligand in serum; these findings help to explain the contribution of TREM-1 during systemic inflammation.

Indexed as

RNA Processing, Post-TranscriptionalAdultCell Culture TechniquesChi-Square DistributionFemaleFlow CytometryHumansInterleukin-10LipopolysaccharidesLymphocyte ActivationMaleMembrane GlycoproteinsMiddle AgedMonocytesReceptors, ImmunologicReverse Transcriptase Polymerase Chain ReactionInterleukin-10LipopolysaccharidesMembrane GlycoproteinsReceptors, ImmunologicRNA, MessengerTREM1 protein, humanTriggering Receptor Expressed on Myeloid Cells-1Tumor Necrosis Factor-alpha

Identifiers

PMID16907912
PMCPMC1809719
OpenAlexW2074487087

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.