My research investigates mechanisms of non‑resolving inflammation in sepsis, acute respiratory distress syndrome (ARDS) and multiple organ failure, conditions for which only limited mechanism‑based therapeutic advances have been achieved in recent decades. To better understand the pathogenesis of these syndromes and to identify new therapeutic targets, we focus on two complementary approaches that we consider particularly promising: defining the programs of resolution of inflammation and innate immune regulation that fail in critically ill patients, and delineating how immunoresilience and immunometabolism can be harnessed to restore protective host responses and prevent organ failure.
My laboratory uses both hypothesis‑driven and unbiased experimental strategies to address two central questions:
• What drives the acute and dysregulated activation of the innate immune system in sepsis and ARDS, and why do endogenous mechanisms of inflammatory resolution fail? • How do neuronal guidance proteins (NGPs) and associated signaling pathways shape inflammatory networks, tissue injury and regeneration, and can these pathways be targeted for therapeutic benefit in critically ill patients?
By dissecting both established and novel circuits in innate immunity, resolution biology and immunometabolism, my research aims to define pro‑resolving pathways and disease‑relevant targets that can inform the development of new, mechanism‑based therapies in translational intensive care medicine.
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