The Gram-positive bacterium Listeria monocytogenes is an opportunistic food-borne pathogen infecting Mammalian organisms. As such, it has the ability to cross epithelial barriers and to multiply in the host, leading to severe illness in immunocompromised individuals (septicaemia, meningitidis), to pregnancy failures, and to neonatal pathologies in newborn child (see for instance the 2017 EFSA & ECDC report, or the proceedings of the 2016 International Symposium on Problems of Listeria and Listeriosis).

Listeria monocytogenes is a facultative intracellular pathogen. It can enter into the host cytoplasm and multiply there, using a variety of bacterial effectors in order to hijack the host cellular machinery to its own benefit. For instance, this bacterium is able to polymerise actin, a component of the cell cytoskeleton, which allows its motility throughout the infected cell (Gouin E et al. Curr. Opin. Microbiol., 2005).

Over the past decades, the molecular mechanisms underlying the intracellular life of Listeria have been thoroughly explored. By doing so, cellular microbiologists have brought an important contribution to the understanding of a number of key cellular processes, which can be subverted by bacteria but are also relevant for normal cellular physiology (reviewed in Radoshevich & Cossart, Nat. Rev. Microbiol., 2017).