Abstract
We developed a 2D multi-agent stochastic model of interaction between cellular debris, bacteria and neutrophils in the surface cutaneous wound with local hypoxia. Bacteria, which grow logistically with a maximum carrying capacity, and debris are phagocytosed by neutrophils with probability determined by the partial pressure of oxygen in the tissue, pO 2 = 4–400 mmHg, according to the Michaelis-Menten equation with K m = 40 mmHg. The influx of new neutrophils depends linearly (k = 0.05–0.2) on the amount of (a) platelets and (b) neutrophils, which are in contact with bacteria or debris. Each activated neutrophil can accomplish a certain amount of phagocytosis, n max = 5–20, during its lifespan, T = 1–5 days. The universe of outcomes consists of (a) bacteria clearance (high k and n max ), (b) infection is not cleared by neutrophils (low k and nmax), and (c) intermittent (quasiperiodic) bursts of inflammation. In the absence of infection, phagocytosis stops within 48 h. We found that pO 2 alone did not change the type of outcome, but affects the number of recruited neutrophils and inflammation duration (in the absence of infection by up to 10 and 5 %, respectively).
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Saiko, G., Cross, K., Douplik, A. (2016). Mathematical Model of an Innate Immune Response to Cutaneous Wound in the Presence of Local Hypoxia. In: Luo, Q., Li, L., Harrison, D., Shi, H., Bruley, D. (eds) Oxygen Transport to Tissue XXXVIII. Advances in Experimental Medicine and Biology, vol 923. Springer, Cham. https://doi.org/10.1007/978-3-319-38810-6_56
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DOI: https://doi.org/10.1007/978-3-319-38810-6_56
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