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

Inflammation 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...

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Veröffentlicht in:	PloS one 2010-02, Vol.5 (2), p.e9249
Hauptverfasser:	Dong, Xu, Foteinou, Panagiota T, Calvano, Steven E, Lowry, Stephen F, Androulakis, Ioannis P
Format:	Artikel
Sprache:	eng
Schlagworte:	Acute Disease Agent-based models Analysis Bioinformatics Biomedical engineering Cascades Complexity Computational Biology/Systems Biology Computational Biology/Transcriptional Regulation Computer simulation Critical Care and Emergency Medicine/Sepsis and Multiple Organ Failure Cytokines Dynamic tests Dynamical systems Endotoxins Endotoxins - administration & dosage Endotoxins - immunology Gene Expression Profiling Genes Heterogeneity Human behavior Humans Immune system Immune System - drug effects Immune System - immunology Immunological tolerance Inflammation Inflammation - blood Inflammation - chemically induced Inflammation - immunology Inflammatory response Intracellular signalling Kinases Leukocytes Leukocytes - drug effects Leukocytes - immunology Leukocytes - metabolism Lipopolysaccharides - administration & dosage Lipopolysaccharides - immunology Macrophages - drug effects Macrophages - immunology Macrophages - metabolism Metabolism Models, Immunological NF-kappa B - metabolism Nonlinear dynamics Nonlinear response Nonlinear systems Phosphorylation Physiological aspects Potentiation Propagation Protein Binding - drug effects Rodents Sepsis Signal transduction Signal Transduction - drug effects Signal Transduction - immunology Simulation Software Stochasticity Surgery Th1 Cells - drug effects Th1 Cells - immunology Th1 Cells - metabolism Th2 Cells - drug effects Th2 Cells - immunology Th2 Cells - metabolism Toll-Like Receptor 4 - metabolism Transcription Transcription factors Transcription, Genetic - drug effects
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