An Autonomous Multi-Agent Simulation Model for Acute Inflammatory Response

An Autonomous Multi-Agent Simulation Model for Acute Inflammatory Response

John Wu (Kansas State University, USA), David Ben-Arieh (Kansas State University, USA) and Zhenzhen Shi (Kansas State University, USA)
Copyright: © 2011 |Pages: 17
DOI: 10.4018/jalr.2011040106
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Abstract

This research proposes an agent-based simulation model combined with the strength of systemic dynamic mathematical model, providing a new modeling and simulation approach of the pathogenesis of AIR. AIR is the initial stage of a typical sepsis episode, often leading to severe sepsis or septic shocks. The process of AIR has been in the focal point affecting more than 750,000 patients annually in the United State alone. Based on the agent-based model presented herein, clinicians can predict the sepsis pathogenesis for patients using the prognostic indicators from the simulation results, planning the proper therapeutic interventions accordingly. Impressively, the modeling approach presented creates a friendly user-interface allowing physicians to visualize and capture the potential AIR progression patterns. Based on the computational studies, the simulated behavior of the agent–based model conforms to the mechanisms described by the system dynamics mathematical models established in previous research.
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Biological Mechanism Of Acute Inflammatory Response

Process Description

The Acute Inflammatory Response, which can be the initial stage of sepsis, usually occurs when the human immune system detects intruding pathogens or existing tissue damages and sends out a signal (e.g., Interleukin-8 (IL-8) and C5a, the process is referred to as the chemotaxis) to the resting phagocyte cells such as the neutrophils initially and followed by the monocytes (two typical immune cells in the human body) in the blood vessel near the infected tissue. The resting phagocyte cells are activated and start to migrate towards the pathogens or damaged tissue whose recognizable protein on the surface is similar to those of the immune cells. Once the activated phagocyte cells reach the infection site, they start to engulf and consume the pathogens. Meanwhile, these activated phagocyte cells release pro-inflammatory cytokines such as Tumor Necrosis Factor (TNF), Interleukins (IL-1), IL-6, IL-8 and High Mortality Group Box-1 (HMGB-1) that activate more phagocyte cells and recruit them to the infection site. All those activated phagocyte cells not only eliminate the pathogens but also secrete substances which contribute to killing healthy cells and induce more inflammation in the initial progression of sepsis. Almost at the same time, several types of anti-inflammatory mediators such as IL-6, IL-10, soluble TNF receptors (sTNFRs) and IL-1 receptor antagonist (IL-1ra) are also released by the activated phagocyte cells in this stage. These anti-inflammatory mediators inhibit the production of pro-inflammatory mediators and therefore inhibit recruiting more phagocyte cells (Gogos, 2000).

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