Evidence map›Paper›PMID 28824640›Full record

ArticleFrontiers in immunology2017

A System Dynamics Model to Predict the Human Monocyte Response to Endotoxins.

Enrique Álvarez, Víctor Toledano, Fernando Morilla, Enrique Hernández-Jiménez, Carolina Cubillos-Zapata, Aníbal Varela-Serrano, José Casas-Martín, José Avendaño-Ortiz, Luis A Aguirre, Francisco Arnalich and 4 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2017. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
  3. Article
  4. A review of inflammatory mechanism in airway diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
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

14 authors.

Enrique ÁlvarezInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.
Víctor ToledanoInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.
Fernando MorillaDepartment of Information Technology and Automation, ETSI Information Technology, National University of Distance Learning UNED, Madrid, Spain.
Enrique Hernández-JiménezInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.
Carolina Cubillos-ZapataInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.
Aníbal Varela-SerranoInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.
José Casas-MartínInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.
José Avendaño-OrtizInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.
Luis A AguirreInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.
Francisco ArnalichInternal Medicine Service, La Paz University Hospital, Madrid, Spain.
Charbel Maroun-EidDepartment of Emergency, La Paz University Hospital, Madrid, Spain.
Alejandro Martín-QuirósDepartment of Emergency, La Paz University Hospital, Madrid, Spain.
Manuel Quintana DíazDepartment of Emergency, La Paz University Hospital, Madrid, Spain.
Eduardo López-CollazoInnate Immunity Group, IdiPAZ, La Paz University Hospital, Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

System dynamics is a powerful tool that allows modeling of complex and highly networked systems such as those found in the human immune system. We have developed a model that reproduces how the exposure of human monocytes to lipopolysaccharides (LPSs) induces an inflammatory state characterized by high production of tumor necrosis factor alpha (TNFα), which is rapidly modulated to enter into a tolerant state, known as endotoxin tolerance (ET). The model contains two subsystems with a total of six states, seven flows, two auxiliary variables, and 14 parameters that interact through six differential and nine algebraic equations. The parameters were estimated and optimized to obtain a model that fits the experimental data obtained from human monocytes treated with various LPS doses. In contrast to publications on other animal models, stimulation of human monocytes with super-low-dose LPSs did not alter the response to a second LPSs challenge, neither inducing ET, nor enhancing the inflammatory response. Moreover, the model confirms the low production of TNFα and increased levels of C-C motif ligand 2 when monocytes exhibit a tolerant state similar to that of patients with sepsis. At present, the model can help us better understand the ET response and might offer new insights on sepsis diagnostics and prognosis by examining the monocyte response to endotoxins in patients with sepsis.

Indexed as

bacterial lipopolysaccharideendotoxin toleranceinflammationmathematical modelmonocytes

Identifiers

PMID28824640
PMCPMC5540970

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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.