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Candida albicans  and  C. parapsilosis  are human pathogens causing severe infections. The NLRP3 inflammasome plays a crucial role in host defence against  C. albicans , but it has been previously unknown whether  C. parapsilosis  activates this complex. Here we show that  C. parapsilosis  induces caspase-1 activation and interleukin-1β (IL-1β) secretion in THP-1, as well as primary, human macrophages. IL-1β secretion was dependent on NLRP3, K + -efflux, TLR4, IRAK, Syk, caspase-1, caspase-8 and NADPH-oxidase. Importantly, while  C. albicans  induced robust IL-1β release after 4 h,  C. parapsilosis  was not able to stimulate the production of IL-1β after this short incubation period. We also found that  C. parapsilosis  was phagocytosed to a lesser extent, and induced significantly lower ROS production and lysosomal cathepsin B release compared to  C. albicans , suggesting that the low extent of inflammasome activation by  C. parapsilosis  may result from a delay in the so-called “signal 2”. In conclusion, this is the first study to examine the molecular pathways responsible for the IL-1β production in response to a non-albicans  Candida  species, and these results enhance our understanding about the immune response against  C. parapsilosis .

Specific pathways mediating inflammasome activation by Candida parapsilosis