Evidence map›Paper›PMID 20174629›Full record

ArticlePloS one2010

Agent-based modeling of endotoxin-induced acute inflammatory response in human blood leukocytes.

Xu Dong, Panagiota T Foteinou, Steven E Calvano, Stephen F Lowry, Ioannis P Androulakis

Abstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Embracing complexity in sepsis.Critical care (London, England) · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Trends in mathematical modeling of host-pathogen interactions.Cellular and molecular life sciences : CMLS · 2020
    Review
  10. Article
  11. A review of inflammatory mechanism in airway diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Bridging Systems Medicine and Patient Needs.CPT: pharmacometrics & systems pharmacology · 2015
    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

5 authors.

Xu DongDepartment of Biomedical Engineering, Rutgers University, Piscataway, New Jersey, United States of America.
Panagiota T Foteinou
Steven E Calvano
Stephen F Lowry
Ioannis P Androulakis

Funding

HORMONE AND CYTOKINE REGULATION OF ENDOTOXIN INJURY(RMI)R37GM034695 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI LOWRY, STEPHEN F · 1997 to 2006
$4.0M
SKELETAL MUSCLE PROTEIN RESPONSE TO INJURY AND REPLETIONR01GM034695 · NIGMS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI CORBETT, SIOBHAN A · 1985 to 2011
$2.8M
NIGMS NIH HHS GM34695NIGMS NIH HHS R01 GM034695NIGMS NIH HHS R37 GM034695
6 · The paper itself

Abstract

backgroundInflammation is a highly complex biological response evoked by many stimuli. A persistent challenge in modeling this dynamic process has been the (nonlinear) nature of the response that precludes the single-variable assumption. Systems-based approaches offer a promising possibility for understanding inflammation in its homeostatic context. In order to study the underlying complexity of the acute inflammatory response, an agent-based framework is developed that models the emerging host response as the outcome of orchestrated interactions associated with intricate signaling cascades and intercellular immune system interactions. METHODOLOGY/PRINCIPAL

findingsAn agent-based modeling (ABM) framework is proposed to study the nonlinear dynamics of acute human inflammation. The model is implemented using NetLogo software. Interacting agents involve either inflammation-specific molecules or cells essential for the propagation of the inflammatory reaction across the system. Spatial orientation of molecule interactions involved in signaling cascades coupled with the cellular heterogeneity are further taken into account. The proposed in silico model is evaluated through its ability to successfully reproduce a self-limited inflammatory response as well as a series of scenarios indicative of the nonlinear dynamics of the response. Such scenarios involve either a persistent (non)infectious response or innate immune tolerance and potentiation effects followed by perturbations in intracellular signaling molecules and cascades. CONCLUSIONS/SIGNIFICANCE: The ABM framework developed in this study provides insight on the stochastic interactions of the mediators involved in the propagation of endotoxin signaling at the cellular response level. The simulation results are in accordance with our prior research effort associated with the development of deterministic human inflammation models that include transcriptional dynamics, signaling, and physiological components. The hypothetical scenarios explored in this study would potentially improve our understanding of how manipulating the behavior of the molecular species could manifest into emergent behavior of the overall system.

Indexed as

Models, ImmunologicalAcute DiseaseEndotoxinsGene Expression ProfilingHumansImmune SystemInflammationLeukocytesLipopolysaccharidesMacrophagesNF-kappa BProtein BindingSignal TransductionSoftwareTh1 CellsTh2 CellsEndotoxinsLipopolysaccharidesNF-kappa BToll-Like Receptor 4

Identifiers

PMID20174629
PMCPMC2823776

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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.