Precision medicine with a focus on reducing organ damage after sepsis

Sepsis is a leading cause of mortality in intensive care units and is estimated to contribute to up to 19% of all deaths worldwide.

The recent Sepsis-3 guidelines define the syndrome as life-threatening organ dysfunction caused by a dysregulated host response to infection.

Recent reports suggest that aberrant mitochondrial pathways, leading to metabolic deregulation in organs, contributes to septic organ dysfunction.

In this project, I plan to use in vitro and in vivo model systems, combined with patient samples and advanced methods in proteomics, metabolomics and structural mass spectrometry to investigate if reducing the amount of mitochondrial stress, referred to as mitohormesis, in combination with broad-spectrum antibiotics can be used as a novel therapeutic strategy to reduce organ damage after sepsis.

The project also aims at aiding in the departure from the prevailing one-size-fits-all paradigm in sepsis to search for treatment indicative biomarkers in sepsis patients focusing on the level of mitochondrial activation.

The long-term ambition of this project is to construct an extendable world-wide unique resource of proteome maps from clinical sepsis samples to generate molecular phenotypes that can be used to i) discover molecular patterns for improved patient stratification, ii) narrow the gap between animal models of infection and humans, and iii) identify markers associated with favorable intervention effects.