Abstract
Legionella pneumophila is a facultative intracellular pathogen capable of replicating within a broad range of hosts. One unique feature of this pathogen is the cohort of ca. 300 virulence factors (effectors) delivered into host cells via its Dot/Icm type IV secretion system. Study of these proteins has produced novel insights into the mechanisms of host function modulation by pathogens, the regulation of essential processes of eukaryotic cells and of immunosurveillance. In this review, we will briefly discuss the roles of some of these effectors in the creation of a niche permissive for bacterial replication in phagocytes and recent advancements in the dissection of the innate immune detection mechanisms by challenging immune cells with L. pneumophila.
Highlights
The discovery of Legionella pneumophila dates back to 1976, when a mysterious disease affected 221 American veterans attending the American Legion Convention in Philadelphia
One salient feature associated with L. pneumophila infection is that the bacterial phagosome does not undergo the default phagosomal matu
Ration process characterized by fusion with the lysosomal network, in the early phase of infection; rather it develops into an organelle permissive for intracellular bacterial replication termed the Legionella-containing vacuole (LCV) (Ensminger and Isberg, 2009; Horwitz, 1983; Tilney et al, 2001) (Figure 1)
Summary
Legionella pneumophila is a facultative intracellular pathogen capable of replicating within a broad range of hosts. 300 virulence factors (effectors) delivered into host cells via its Dot/Icm type IV secretion system. Study of these proteins has produced novel insights into the mechanisms of host function modulation by pathogens, the regulation of essential processes of eukaryotic cells and of immunosurveillance. We will briefly discuss the roles of some of these effectors in the creation of a niche permissive for bacterial replication in phagocytes and recent advancements in the dissection of the innate immune detection mechanisms by challenging immune cells with L. pneumophila. Type IV secretion, inflammasome, effectors, posttranslational modification, vesicle transport
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