Toward Understanding the Causes of Rapid Clearance of Staphylococcus aureus During Peritoneal Infection

Abstract

It has been recently shown that fibrinogen, a key component in the blood clotting process, can induce rapid clearance of S. aureus infections in the case of peritoneal infections in mice [1]. Clearance of these bacteria require the interplay of the innate immune response and the presence of fibrinogen, but the relative importance of these mechanisms is poorly understood. In this thesis, we propose several mathe- matical models of S. aureus growth with immune cell interactions and a model of fibrin polymerization to better understand how each individual component contributes to the clearance of bacteria. With each model iteration, we include a new mechanism and parameterize the submodels with experimental data. We find that the full model with all mechanisms in place qualitatively matches experimental findings, and explore parameter identifiability in the model.