What is it about?
We built a mathematical model of arachidonic acid metabolic pathway in inflammatory cells, producing eicosanoids - prostaglandins and leukotrienes. Based on the differences in enzyme expressions of two enzymes in this pathway we defined model 5 populations simulating non-asthmatics as well as one aspirin tolerant and 3 intolerant asthmatic populations. Simulations were carried out for two states of the model - state of no-inflammation and inflammation. Model results were compared with the measured ones and new predictions were proposed. Especially, the dynamic eicosanoid production was predicted in response to NSAIDs for different model populations and the model states of no-inflammation and inflammation. In this way, the sensitiviy to NSAIDs of each model population was investigated.
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Why is it important?
In spite of accumulating experimental and clinical results the molecular and cellular mechanisms, which induce and initiate processes in aspirin induced asthma, are still not completely elucidated and understood. In the past, experimental and clinical research was primarily focused on a single level, either on concerning the gene, molecular, cellular or tissue/organ level. Theoretical analyses and predictions attained from mathematical models, such as ours, integrate the accumulated knowledge of these different levels of research. Therefore, the mathematical model analysis might serve as suitable tool aiding to figure out and test new hypotheses, check molecular mechanisms, analyse experimental results, guide novel experiments as well as give ideas for new methods and tools for diagnosing and treatment diseases on a multiscale level.
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This page is a summary of: Dynamic model of eicosanoid production with special reference to non-steroidal anti-inflammatory drug-triggered hypersensitivity, IET Systems Biology, October 2015, the Institution of Engineering and Technology (the IET),
DOI: 10.1049/iet-syb.2014.0037.
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