title: Cutting edge: Candida albicans hyphae formation triggers activation of the Nlrp3 inflammasome.
abstract: The proinflammatory cytokine IL-1beta plays an important role in antifungal immunity; however, the mechanisms by which fungal pathogens trigger IL-1beta secretion are unclear. In this study we show that infection with Candida albicans is sensed by the Nlrp3 inflammasome, resulting in the subsequent release of IL-1beta. The ability of C. albicans to switch from a unicellular yeast form into a filamentous form is essential for activation of the Nlrp3 inflammasome, as C. albicans mutants incapable of forming hyphae were defective in their ability to induce macrophage IL- 1beta secretion. Nlrp3-deficient mice also demonstrated increased susceptibility to infection with C. albicans, which is consistent with a key role for Nlrp3 in innate immune responses to the pathogen C. albicans.
authors.affiliation: Division of Infectious Diseases, University of Iowa, Iowa City, IA 52242, USA.
authors.forename: Sophie
authors.initials: S
authors.lastname: Joly
authors.forename: Ning
authors.initials: N
authors.lastname: Ma
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Sadler
authors.forename: David R
authors.initials: DR
authors.lastname: Soll
authors.forename: Suzanne L
authors.initials: SL
authors.lastname: Cassel
authors.forename: Fayyaz S
authors.initials: FS
authors.lastname: Sutterwala
mesh_terms: D000818:Animals; D002176:Candida albicans / Q000166:cytology / Q000276:immunology*; D002352:Carrier Proteins / Q000276:immunology*; D004198:Disease Susceptibility / Q000276:immunology; D025301:Hyphae / Q000276:immunology*; D007109:Immunity; D053583:Interleukin-1beta / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein
chemical_list: D002352:Carrier Proteins; D053583:Interleukin-1beta; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C492716:Nlrp3 protein, mouse
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