AUTHOR=Swart A. Leoni , Hilbi Hubert 

TITLE=Phosphoinositides and the Fate of Legionella in Phagocytes

JOURNAL=Frontiers in Immunology

VOLUME=11

YEAR=2020

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2020.00025

DOI=10.3389/fimmu.2020.00025

ISSN=1664-3224

ABSTRACT=<p><italic>Legionella pneumophila</italic> is the causative agent of a severe pneumonia called Legionnaires' disease. The environmental bacterium replicates in free-living amoebae as well as in lung macrophages in a distinct compartment, the <italic>Legionella</italic>-containing vacuole (LCV). The LCV communicates with a number of cellular vesicle trafficking pathways and is formed by a plethora of secreted bacterial effector proteins, which target host cell proteins and lipids. Phosphoinositide (PI) lipids are pivotal determinants of organelle identity, membrane dynamics and vesicle trafficking. Accordingly, eukaryotic cells tightly regulate the production, turnover, interconversion, and localization of PI lipids. <italic>L. pneumophila</italic> modulates the PI pattern in infected cells for its own benefit by (i) recruiting PI-decorated vesicles, (ii) producing effectors acting as PI interactors, phosphatases, kinases or phospholipases, and (iii) subverting host PI metabolizing enzymes. The PI conversion from PtdIns(3)<italic>P</italic> to PtdIns(4)<italic>P</italic> represents a decisive step during LCV maturation. In this review, we summarize recent progress on elucidating the strategies, by which <italic>L. pneumophila</italic> subverts host PI lipids to promote LCV formation and intracellular replication.</p>