SP30 Mitochondrial Dynamics in Innate Immune Training
Project leader: Sebastian Weis
Doctoral candidate: Lea Hauswald
Mitochondria fulfill major cellular tasks beyond ATP production such as assembly of iron-sulphur clusters, heme biosynthesis, control of metabolic pathways and regulation apoptosis amongst others (Westermann, 2010). In contrast to previous believes, recent evidence shows that mitochondria are highly dynamic organelles whose activity is influenced by organelle merging, referred to as fusion which creates interconnecting mitochondrial networks adapting to energy requirements (Tondera et al., 2009), organelle shedding referred to as fission and degradation, referred to as mitophagy. We have recently proposed that differential energy investment patterns are determined by pathogen quantities and impact on observed dose dependant response patterns, i.e. training vs. tolerance (Bauer et al., 2018). Furthermore, mitochondrial dynamics critically contribute to the energetic and metabolic demands of the cell. It is therefore conceivable that mitochondrial dynamics directly respond to pathogen numbers. In fact mitochondrial dysfunction has been linked to multi-organ failure in sepsis (Park and Zmijewski, 2017).
In our RTG-associated PhD project, we investigate the hypothesis that innate immune training or tolerance critically involves mitochondrial dynamics controlling the cellular energy homeostasis.