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Serotype 1 and 8 Pneumococci Evade Sensing by Inflammasomes in Human Lung Tissue
Authors:Diana Fatykhova  Anne Rabes  Christoph Machnik  Kunchur Guruprasad  Florence Pache  Johanna Berg  Mario Toennies  Torsten T Bauer  Paul Schneider  Maria Schimek  Stephan Eggeling  Timothy J Mitchell  Andrea M Mitchell  Rolf Hilker  Torsten Hain  Norbert Suttorp  Stefan Hippenstiel  Andreas C Hocke  Bastian Opitz
Abstract:Streptococcus pneumoniae is a major cause of pneumonia, sepsis and meningitis. The pore-forming toxin pneumolysin is a key virulence factor of S. pneumoniae, which can be sensed by the NLRP3 inflammasome. Among the over 90 serotypes, serotype 1 pneumococci (particularly MLST306) have emerged across the globe as a major cause of invasive disease. The cause for its particularity is, however, incompletely understood. We therefore examined pneumococcal infection in human cells and a human lung organ culture system mimicking infection of the lower respiratory tract. We demonstrate that different pneumococcal serotypes differentially activate inflammasome-dependent IL-1β production in human lung tissue and cells. Whereas serotype 2, 3, 6B, 9N pneumococci expressing fully haemolytic pneumolysins activate NLRP3 inflammasome-dependent responses, serotype 1 and 8 strains expressing non-haemolytic toxins are poor activators of IL-1β production. Accordingly, purified haemolytic pneumolysin but not serotype 1-associated non-haemolytic toxin activates strong IL-1β production in human lungs. Our data suggest that the evasion of inflammasome-dependent innate immune responses by serotype 1 pneumococci might contribute to their ability to cause invasive diseases in humans.
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