@entity6026 Triggered by the XXXX Inflammasome Induces Host Innate Resistance in a Pulmonary Model of Fungal Infection.

@entity6026 @entity19 @entity377 @entity12267 @entity281 @entity972 @entity13761 @entity6198
UNASSIGNED: Pathogens are sensed by innate immune receptors that initiate an efficient adaptive immune response upon activation. The elements of the innate immune recognition process for @entity12267 include TLR-2, TLR-4, and dectin-1. However, there are additional receptors necessary for the host immune responses to @entity12267 . The @entity377 -binding oligomerization domain-like receptor (NLRs), which activate inflammasomes, are candidate receptors that deserve renewed investigation. After pathogen @entity281 , the NLRs form large signaling platforms called inflammasomes, which lead to @entity13761 activation and maturation of proinflammatory cytokines ( @entity6026 and IL-1b). In this study, we showed that NLR family pyrin domain-containing 3 ( @entity6198 ) is required to induce @entity13761 activation and further secretion of IL-1b and @entity6026 by @entity12267 -infected macrophages. Additionally, @entity972 efflux and lysosomal acidification induced by the fungus were important steps in the @entity13761 activation mechanism. Notably, @entity6198 and @entity13761 knockout @entity19 were more susceptible to @entity281 than were the wild-type animals, suggesting that the @entity6198 -dependent inflammasomes contribute to host protection against @entity12267 . This protective effect occurred owing to the inflammatory response mediated by @entity6026 , as shown by an augmented fungus burden in @entity6026 knockout @entity19 . Taken together, our results show that the @entity6198 inflammasome is essential for resistance against @entity12267 because it orchestrates robust @entity13761 activation and triggers an @entity6026 -dependent proinflammatory response.
