**1. Introduction**

Bacterial pathogens have evolved diverse and effective strategies to promote their survival in human cells. Some bacteria can circumvent the innate immune response, managing to replicate within macrophages, which are the first line of defense against microbial pathogens and genetically programmed to eradicate foreign particles. Mechanisms that bacteria employ to survive in macrophages include (i) acclimating to the acidic environment within the host lysosome, (ii) escaping the phagosome to persist inside the host cell cytoplasm, and (iii) eluding the endolysosomal pathway by establishing a replication permissive vacuole within the host [1]. The Gram-negative facultative intracellular bacterium, *Legionella pneumophila*, has adopted a survival strategy that relies on the establishment of a protective vacuole that avoids encounters with the endolysosomal pathway. By phagocytosis, macrophages internalize *L. pneumophila* into a membrane-bound compartment termed as phagosome. Upon uptake, *L. pneumophila* directs

membrane remodeling of the phagosomal compartment, employing a sizeable artillery of bacterial proteins that subvert multiple host cellular processes without compromising survival of the host cell throughout infection [2–4]. A specialized secretion system is responsible for translocating these proteins, known as effector proteins, from the bacterial milieu into the host cytosol [5–7]. Effector proteins do not share extensive homology with each other and are often composed of multiple domains that are functionally distinct [8, 9]. An emerging feature among effector proteins is their ability to recognize and bind host phosphoinositides (PIPs) [10], which are a series of phospholipids that play critical roles in coordinating cell signaling and membrane trafficking events in eukaryotic cells [11]. *L. pneumophila* effector proteins exploit the spatiotemporal regulation of host PIPs to facilitate the formation of the *Legionella*-containing vacuole (LCV) and to avoid the endolysosomal pathway. Disruption of the PIP distribution on the LCV membranes leads to bacterial degradation, illustrating that controlling PIP dynamics on and around the LCV is crucial for intracellular survival of *L. pneumophila* [12]. Here we will discuss the *L. pneumophila* effector proteins that contribute to vacuole biogenesis and maintenance through the exploitation of host phosphoinositides.
