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| A complex combination of interactions initiates and regulates the inflammatory phase of the wound healing response. Many chronic wounds arise due to an improper transition out of this phase. To understand regulation of this transition, we developed a model of key interactions involving neutrophils and macrophages during wound healing. This model also accounts for the effects of cortisol, (a stress hormone, elevated post trauma), and estrogen (protective, treatment option) on the activity of these cells. Latin Hypercube sampling was performed to determine biologically feasible parameter sets for this model, which satisfy conditions for stability of the healthy outcome and peak times for these key cell types. Experimental data from Broughton et al (2006) and Lebovich & Ross (1975) was used to validate model results. This model forms the inflammatory subsystem of a wound healing model that accounts for wound dynamics post trauma. |
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