Deciphering the role of spingolipids in bacterial egress

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Infection of eukaryotic host cells with intracellular pathogens is a well-coordinated process. It includes adhesion and invasion of the host cell, establishment of a replicative permissive intracellular niche and the release of infectious progeny from the infected cell. Apart from the well-studied processes invasion and intracellular survival, egress from the host cell is crucial step during infection that has so far not been investigated in depth. Pathogens can leave the host cell by different pathways including lysis of the host cell or by non-lytic processes that result in egress of the pathogen without host cell death. Extrusion formation by Chlamydia species is an example for the latter one. It is currently not well understood how exit pathways are regulated and which factors trigger distinct exit strategies under certain conditions. Especially, the roles of sphingolipids as bioactive lipids regulating cellular pathways including signaling and secretion have not been addressed in the context of non-lytic bacterial egress. Preliminary data of my group suggest that sphingolipids control Chlamydia extrusion formation. In this proposal, we aim to close this knowledge gap by studying the emerging roles of sphingolipids in regulation of extrusion formation of the zoonotic pathogen C. psittaci as a model organism by controlling signaling pathways, membrane dynamics and/or expression and localization of bacterial proteins. Furthermore, the impact of sphingolipids on exit strategies of other pathogens will be studied.