ArticlePLoS computational biology2019
Identifying important parameters in the inflammatory process with a mathematical model of immune cell influx and macrophage polarization.
Article in PLoS computational biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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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.
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Who cites it
20 citing papers in PubMed, 54 citations in OpenAlex.
- Circadian Disruption Exacerbates Innate Immune Responses by Modulating the Bistability of Pro-Inflammatory Signaling: A Dynamical Modeling Study.Biomedicines · 2026Article
- AnACS omega · 2026Article
- Light-Responsive Surface Topographies Modulate Macrophage Immune Responses Through Dynamic Mechanical Cues.Macromolecular bioscience · 2026Article
- Asbestos Disease Initiation.Bulletin of mathematical biology · 2026Article
- Article
- Macrophages at the Crossroads of Chronic Stress and Cancer.International journal of molecular sciences · 2025Review
- Single-cell multi-omics-based immune temporal network resolution in sepsis: unravelling molecular mechanisms and precise therapeutic targets.Frontiers in immunology · 2025Review
- Unraveling host-pathogen dynamics in a murine Model of septic peritonitis induced by vancomycin-resistantVirulence · 2024Article
- Unraveling Macrophage Polarization: Functions, Mechanisms, and "Double-Edged Sword" Roles in Host Antiviral Immune Responses.International journal of molecular sciences · 2024Review
- A systematic evaluation of the influence of macrophage phenotype descriptions on inflammatory dynamics.Mathematical medicine and biology : a journal of the IMA · 2024Article
- Quantitatively Mapping Immune Control during Influenza.Current opinion in systems biology · 2024Article
- Characterization of differences in immune responses during bolus and continuous infusion endotoxin challenges using mathematical modelling.Experimental physiology · 2024Article
- Article
- Exploring the constituent mechanisms of hepatitis: a dynamical systems approach.Mathematical medicine and biology : a journal of the IMA · 2023Article
- Computational Modeling of Macrophage Iron Sequestration during Host Defense against Aspergillus.mSphere · 2022Article
- Mathematical modeling of ventilator-induced lung inflammation.Journal of theoretical biology · 2021Article
- Modeling viral dynamics in SARS-CoV-2 infection based on differential equations and numerical analysis.Heliyon · 2021Article
- Infection, inflammation and intervention: mechanistic modelling of epithelial cells in COVID-19.Journal of the Royal Society, Interface · 2021Article
- A Mathematical Model of the Dynamics of Cytokine Expression and Human Immune Cell Activation in Response to the PathogenFrontiers in cellular and infection microbiology · 2021Article
- A case for the reuse and adaptation of mechanistic computational models to study transplant immunology.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In an inflammatory setting, macrophages can be polarized to an inflammatory M1 phenotype or to an anti-inflammatory M2 phenotype, as well as existing on a spectrum between these two extremes. Dysfunction of this phenotypic switch can result in a population imbalance that leads to chronic wounds or disease due to unresolved inflammation. Therapeutic interventions that target macrophages have therefore been proposed and implemented in diseases that feature chronic inflammation such as diabetes mellitus and atherosclerosis. We have developed a model for the sequential influx of immune cells in the peritoneal cavity in response to a bacterial stimulus that includes macrophage polarization, with the simplifying assumption that macrophages can be classified as M1 or M2. With this model, we were able to reproduce the expected timing of sequential influx of immune cells and mediators in a general inflammatory setting. We then fit this model to in vivo experimental data obtained from a mouse peritonitis model of inflammation, which is widely used to evaluate endogenous processes in response to an inflammatory stimulus. Model robustness is explored with local structural and practical identifiability of the proposed model a posteriori. Additionally, we perform sensitivity analysis that identifies the population of apoptotic neutrophils as a key driver of the inflammatory process. Finally, we simulate a selection of proposed therapies including points of intervention in the case of delayed neutrophil apoptosis, which our model predicts will result in a sustained inflammatory response. Our model can therefore provide hypothesis testing for therapeutic interventions that target macrophage phenotype and predict outcomes to be validated by subsequent experimentation.
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Registered trials
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.