진학프로석·박사 채용 접수 플랫폼

About the project

Sepsis is a severe form of organ dysfunction, with high morbidity and mortality rates, worldwide. Cardiac dysfunction is one of the most common and severe complications of sepsis and directly affects patient mortality, as normal cardiac function is crucial for adequate organ perfusion. How sepsis induces acute cardiomyopathy is complex and characterized by numerous inter- and intra-cellular dysfunctions. The underlying mechanisms leading to cardiomyocyte acute dysfunction in the context of sepsis remains largely elusive. With the emergence of antibiotic-resistant bacteria, the number of individuals affected by bacteria-induced sepsis is bound to increase dramatically, representing an unmet medical need.

The overall objective of our project is to better understand cardiomyocyte death and/or dysfunction and therefore acute cardiac insufficiency in the context of bacterial sepsis, with a focus on N. meningitidis infection. For this, we leverage a consortium expertise in microbiology, vascular biology, cardiac biology, and critical care medicine.

Our main objectives are:(1) to identify factors specifically released by endothelial cells during meningococcal infection that will be involved in lethal sepsis. Will focus on endothelium-derived extracellular vesicles produced as a result of N. meningitidis interaction with endothelial cells, a specific feature of this infection; (2) to define the molecular and cellular impact of meningococcal infection on vascular and cardiac dysfunction, which ultimately leads to animal death.

Research keywords: Cardiovascular Dysfunctions; Endothelium-Derived Microparticles; Host-Pathogen Interactions; Sepsis; Mouse models