Abstract:Legionella pneumophila, the causative agent of the severe pneumonia known as Legionnaires’ disease, uses its IVB secretion system to transport effector proteins into host cells. The effectors interact with host proteins and lipids to form a unique bacterial phagosome, Legionella-containing vacuole (LCV), which is required for the growth of Legionella in host cells. Phosphatidylinositols (PIs), a group of essential lipids for cells, are involved in signal transduction and vesicle transport. The available studies have demonstrated that L. pneumophila uses its effectors to regulate the host PI metabolism and the lipid composition of LCV membrane to promote the LCV maturation. We review the studies about the pathogenesis of L. pneumophila and the modulation of host PI metabolism and the related enzymes by the effectors of L. pneumophila, expecting to provide a reference for further understanding the regulation mechanisms of host lipid metabolism by Legionella.