title: Simulation of Healing Threshold in Strain-Induced Inflammation Through a Discrete Informatics Model.
abstract: Respiratory diseases such as asthma and acute respiratory distress syndrome as well as acute lung injury involve inflammation at the cellular level. The inflammation process is very complex and is characterized by the emergence of cytokines along with other changes in cellular processes. Due to the complexity of the various constituents that makes up the inflammation dynamics, it is necessary to develop models that can complement experiments to fully understand inflammatory diseases. In this study, we developed a discrete informatics model based on cellular automata (CA) approach to investigate the influence of elastic field (stretch/strain) on the dynamics of inflammation and account for probabilistic adaptation based on statistical interpretation of existing experimental data. Our simulation model investigated the effects of low, medium, and high strain conditions on inflammation dynamics. Results suggest that the model is able to indicate the threshold of innate healing of tissue as a response to strain experienced by the tissue. When strain is under the threshold, the tissue is still capable of adapting its structure to heal the damaged part. However, there exists a strain threshold where healing capability breaks down. The results obtained demonstrate that the developed discrete informatics based CA model is capable of modeling and giving insights into inflammation dynamics parameters under various mechanical strain/stretch environments.
authors.forename: Israr Bin M
authors.initials: IBM
authors.lastname: Ibrahim
authors.forename: Sanjay
authors.initials: S
authors.lastname: Sarma O V
authors.forename: Ramana M
authors.initials: RM
authors.lastname: Pidaparti
mesh_terms: D055371:Acute Lung Injury / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D003198:Computer Simulation; D004548:Elasticity; D006801:Humans; D008954:Models, Biological; D011014:Pneumonia / Q000503:physiopathology*; D012038:Regeneration / Q000502:physiology