Sepsis is a life-threatening disease, associated with a severe infection associated and organ dysfunction causing mortality of more than 25–30%, and even 40–50% when septic shock is present. So far, no effective specific anti-sepsis treatments are available and management of sepsis patients relies mainly on early recognition allowing correct therapeutic measures. During disease progression, a disruption of epithelial and endothelial barrier function is a typical pathological change in acute sepsis. Two major mechanisms have to be considered to be responsible for barrier breakdown: Signals generated by the deregulated and overreacting immune system, as well as signals or activities from pathogenic bacteria and fungi directly interacting with epithelial or endothelial cells are assumed to contribute to gut barrier breakdown. Subsequent systemic inflammation leads to the development of acute sepsis and the liver is among the first organs affected.

To investigate the underlying molecular and cellular mechanisms of an inflammation-associated organ dysfunction, Dr. Mosig and his team have developed a human gut-liver axis based on a microfluidically perfused organ-on-chip platform. The in vitro gut-liver axis comprises tissue resident as well as circulating immune cells emulating essential components of the human immune system.

His current work focusses on the integration of an essential bacterial and fungal microbiome to further emulate commensal/pathogen interaction with the host. In his talk, he will present his gut-liver-on-chip system and its use as tool for disease modelling of human sepsis in the context of a disturbed host - microbiome/pathogen interaction.

When: Tuesday, 17th April, 2018, 2.15 pm - 3.30 pm

Where: Technical University of Berlin, Institute of Biotechnology, Building 17A, Gustav-Meyer-Allee 25, 13355 Berlin, Room: 478