Working together to fighting the bad guys.

Abstract

When Sabine Ehrt first got into contact with bacteria in University lectures, she almost disregarded them as being too simple. But soon she realised that ‘they are actually not that simple; they are quite complicated, adapting to different environments, niches, and hosts.’ After finishing her Ph.D. on adaptation strategies of Acinetobacter calcoaceticus at the University of Erlangen in Germany, Sabine switched to human pathogens for her postdoc positions at Cornell University Medical College in New York and the University of California at Berkeley. She took the chance to work on bacteria that require a biosafety 3 lab set up and deep dived into the question of how the death-causing pathogen Mycobacterium tuberculosis adapts to humans. As an Assistant Professor in the Department of Microbiology and Immunology at Weill Medical College of Cornell University, Sabine started a substantial collaboration with Dirk Schnappinger to investigate the pathogen’s adaptation mechanisms. Mycobacterium tuberculosis comes into contact with a host via inhalation and infects macrophages in the lung. Within the macrophage cytosol, the pathogen resides within phagosomes, but prevents them from fusing with lysosomes and thereby from clearing the pathogen. To investigate how the pathogen adjusts to the macrophage environment and how macrophages respond to the infection, Sabine and her team set up two major studies ‘that used microarray techniques for the first time in tuberculosis research’. They found that M. tuberculosis senses the intraphagosomal environment through the presence of fatty acids and low pH. Hence, the pathogen responds by inducing anaerobic respiration, degradation of fatty acids, remodelling of its cell envelope and by producing siderophores for efficient iron acquisition (Schnappinger et al. 2003). Similarly, macrophages upregulate genes with functions related to immunity and inflammation to clear the invading pathogen. About 25% of the macrophage genome showed altered expression levels upon infection mainly driven by the macrophage-activating factor Interferon-γ (Ehrt et al. 2001). Her collaborative spirit became even more profound when Sabine was appointed Professor in 2010. She got involved in several global scientific projects, e.g. as chair of the Tuberculosis/Leprosy Panel of the USA–Japan Cooperative Medical Science Program, which fosters engagement between US and Asian scientists. Sabine was also involved on scientific advisory boards of several international research programs, including the Translational & Clinical Research Flagship Program Medical Research Council Singapore and the Research Unit at the University of Witwatersrand in Johannesburg. Being a member of the European Academy of Microbiology and section editor of their journal microLife fosters her belief that ‘science is and should not be limited to a single country or continent as it is important to collaborate with other scientists globally and exchange knowledge’.