Schell U Simon S Hilbi H 2016 The Gram-negative bacterium Legionella pneumophila colonizes extracellular environmental niches and infects free-living protozoa. Upon inhalation into the human lung, the opportunistic pathogen grows in macrophages and causes a fulminant pneumonia termed Legionnaires' disease. L. pneumophila employs a biphasic life cycle, comprising a replicative, non-virulent, and a stationary, virulent form. In the latter phase, the pathogen produces a plethora of so-called effector proteins, which are injected into host cells, where they subvert pivotal processes and promote the formation of a distinct membrane-bound compartment, the Legionella-containing vacuole. In the stationary phase, the bacteria also produce a single monopolar flagellum and become motile. L. pneumophila flagellin is recognized by and triggers the host's NAIP5 (Birc1e)/NLRC4 (Ipaf) inflammasome, which leads to caspase-1 activation, pore formation, and pyroptosis. The production of L. pneumophila flagellin and pathogen-host interactions are controlled by a complex stationary phase regulatory network, detecting nutrient availability as well as the Legionella quorum sensing (Lqs) signaling compound LAI-1 (3-hydroxypentadecane-4-one). Thus, the small molecule LAI-1 coordinates L. pneumophila flagellin production and motility, inflammasome activation, and virulence. https://sonar.ch/global/documents/298472 eng info:eu-repo/semantics/altIdentifier/doi/10.1007/978-3-319-41171-2_8 info:eu-repo/semantics/altIdentifier/pmid/27460809 Current topics in microbiology and immunology. - 2016 Amoeba Autoinducer Dictyostelium Effector protein Flagellin Macrophage NAIP5/NLRC4 inflammasome Pathogen vacuole Phosphoinositide Quorum sensing Small GTPase Type IV secretion Animals Flagella Host-Pathogen Interactions Humans Inflammasomes Legionella pneumophila Legionnaires' Disease Inflammasome Recognition and Regulation of the Legionella Flagellum. http://purl.org/coar/resource_type/c_6501