ArticleMolecular medicine (Cambridge, Mass.)
In silico and in vivo approach to elucidate the inflammatory complexity of CD14-deficient mice.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 78 citations in OpenAlex.
- Central role for MCP-1/CCL2 in injury-induced inflammation revealed by in vitro, in silico, and clinical studies.PloS one · 2013Trial
- Towards systems immunology of critical illness at scale: from single cell 'omics to digital twins.Trends in immunology · 2023Review
- Complex Stability and an Irrevertible Transition Reverted by Peptide and Fibroblasts in a Dynamic Model of Innate Immunity.Frontiers in immunology · 2019Article
- Inflammation and Disease: Modelling and Modulation of the Inflammatory Response to Alleviate Critical Illness.Current opinion in systems biology · 2018Article
- Reverse Engineering the Inflammatory "Clock": From Computational Modeling to Rational Resetting.Drug discovery today. Disease models · 2016Article
- Inflammation Following Traumatic Brain Injury in Humans: Insights from Data-Driven and Mechanistic Models into Survival and Death.Frontiers in pharmacology · 2016Article
- Insights into the Role of Chemokines, Damage-Associated Molecular Patterns, and Lymphocyte-Derived Mediators from Computational Models of Trauma-Induced Inflammation.Antioxidants & redox signaling · 2015Review
- The inverse problem in mathematical biology.Mathematical biosciences · 2015Review
- Global sensitivity analysis of a mathematical model of acute inflammation identifies nonlinear dependence of cumulative tissue damage on host interleukin-6 responses.Journal of theoretical biology · 2014Article
- Computational modelling of the inflammatory response in trauma, sepsis and wound healing: implications for modelling resilience.Interface focus · 2014Review
- A mathematical model of intrahost pneumococcal pneumonia infection dynamics in murine strains.Journal of theoretical biology · 2014Article
- In silico modeling: methods and applications to trauma and sepsis.Critical care medicine · 2013Review
- Combined in silico, in vivo, and in vitro studies shed insights into the acute inflammatory response in middle-aged mice.PloS one · 2013Article
- Sepsis: Something old, something new, and a systems view.Journal of critical care · 2012Article
- A two-compartment mathematical model of endotoxin-induced inflammatory and physiologic alterations in swine.Critical care medicine · 2012Article
- Sepsis: from pattern to mechanism and back.Critical reviews in biomedical engineering · 2012Review
- Pharmacokinetic/pharmacodynamic modeling in inflammation.Critical reviews in biomedical engineering · 2012Review
- Linking Inflammation, Cardiorespiratory Variability, and Neural Control in Acute Inflammation via Computational Modeling.Frontiers in physiology · 2012Article
- Fixed volume or fixed pressure: a murine model of hemorrhagic shock.Journal of visualized experiments : JoVE · 2011Article
- An agent-based model of inflammation and fibrosis following particulate exposure in the lung.Mathematical biosciences · 2011Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
The inflammatory phenotype of genetically modified mice is complex, and the role of Gram-negative lipopolysaccharide (LPS) in acute inflammation induced by surgical cannulation trauma, alone or in combination with hemorrhage and resuscitation ("hemorrhagic shock"), is both complex and controversial. We sought to determine if a mathematical model of acute inflammation could elucidate both the phenotype of CD14-deficient (CD14(-/-)) mice--following LPS, cannulation, or hemorrhagic shock--and the role of LPS in trauma/hemorrhage-induced inflammation. A mathematical model of inflammation initially calibrated in wild-type (C57Bl/6) mice subjected to LPS, cannulation, and hemorrhagic shock was recalibrated in CD14(-/-) mice subjected to the same insults, yielding an ensemble of models that suggested specific differences at the cellular and molecular levels (for example, 43-fold lower activation of leukocytes by LPS). The CD14(-/-)-specific model ensemble could account for complex changes in inflammatory analytes in these mice following LPS treatment. Model prediction of similar organ damage in CD14(-/-) and wild-type mice subjected to cannulation alone or with hemorrhagic shock was verified in vivo (similar ALT levels). These studies suggest that LPS-CD14 responses do not cause inflammation in surgical trauma/hemorrhagic shock and demonstrate a novel use of combined in silico and in vivo methods to elucidate the complex inflammatory phenotype of genetically modified animals.
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