The haemostatic system is increasingly recognized as an integral component of innate immunity that not only prevents bleeding but also shapes host–pathogen interactions during infection. While dysregulated coagulation contributes to organ failure in sepsis, local activation of coagulation and protease networks at sites of infection can restrict pathogen dissemination and modulate disease progression.

Our research investigates how host-derived proteases and coagulation factors functionally regulate bacterial virulence and invasive potential. We focus on the proteolytic microenvironment that arises during infection through and local coagulation and neutrophil activation, and how this environment modifies bacterial factors associated with tissue invasion and dissemination.

By integrating microbiology, immunology, and haemostasis research, we aim to understand how host responses both contain and inadvertently promote invasive disease. A central goal is to identify mechanisms that determine the transition from localized infection to systemic pathology and to uncover novel targets for adjunctive therapies in severe bacterial infections.