Abstract
Tuberculosis (TB) has a long history as a serious disease induced by its causative agent Mycobacterium tuberculosis. This pathogen manipulates the host’s immune response, thereby stimulating inflammatory processes, which leads to an even greater imbalance of specific enzymes/inhibitors that contribute to tissue destruction. This work addresses a model consisting of two ordinary differential equations obtained by reducing a previously developed large-scale model describing lung damage, taking into account key metabolic pathways controlled by bacteria. The resulting system is explored as a dynamical system simulating the interaction between bio-markers (matrix metalloproteinases) of tissue destruction and the pathogen. In addition to the analysis of the mathematical model’s features, we qualitatively compared the model dynamics with real clinical data and discussed their mutual correspondence.
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