Visceral leishmaniasis (also called "Kala-azar") is a widespread disease, which is usually fatal in the absence of treatment. Characteristic of the liver immune response to leishmaniasis is a type of inflammation (granulomatous inflammation) that leads to the formation of "granulomas". A granuloma provides a very interesting micro-environment, which is maintained by the coordination
of many cells of the immune system.
Due to the complexity of the immune response, only a limited amount of modeling work exists in the context of granulomatous infection, and most of the current models focus only on the formation stage of granulomas.
The primary goal of this thesis is to gain insights into the process of formation and development of a granuloma. To this end, we built a model of the granuloma formation and resolution in the liver using stochastic Petri nets, and performed several in silico experiments to study the nature of the immune response to leishmaniasis, possible therapeutic options, and the role of the cells involved.
Additionally, the building of the model is extensively documented, and the most important qualitative and quantitative assumptions are referenced and discussed, with the aim of presenting a \u201cconceptual framework\u201d to be used when facing similar problems. The model is validated against available biological data, and its robustness is assessed using sensitivity analysis
