Inflammation is a process driven by underlying cell-cell communication and many other factors. In this study, a model of cell-cell communications was proposed to study factors driving the inflammation time course. Analyses of inflammations that are driven by the combined effects of strain (mechanical stimuli) and/or pathogens are considered in this paper. An agent-based model was employed to simulate inflammation where macrophages and fibroblasts influence each other through cell signaling cytokines that diffuse and spread in the tissue space. The communication network of macrophages and fibroblasts was then inferred and its network model (termed TE network) was generated and analyzed. The results suggest that factors driving inflammation time course can be discriminated by the characteristics of TE networks. Inflammation driven only by pathogens has certain TE network characteristics indicating slower and lower information exchange among cells. Multiple stimuli can help to maintain sufficient information exchange among cells, which is beneficial for inflammation resolution. The TE network captures the unfolding of the innate immune system over time, and the history of pathogens invasion. The resulting network leads to an improved understanding of the resilience of the system to future pathogen invasion.
Keywords: cell communication; inflammation; network.