Inflammasome Recognition and Regulation of the Legionella Flagellum.
Curr Top Microbiol Immunol
; 397: 161-81, 2016.
Article
en En
| MEDLINE
| ID: mdl-27460809
ABSTRACT
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.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Enfermedad de los Legionarios
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Legionella pneumophila
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Inflamasomas
/
Flagelos
Límite:
Animals
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Humans
Idioma:
En
Año:
2016
Tipo del documento:
Article