Specific pathways mediating inflammasome activation by Candida parapsilosis
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...
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Dokumentumtípus: | Cikk |
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Nature Publishing Group
2017
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Sorozat: | SCIENTIFIC REPORTS
7 |
doi: | 10.1038/srep43129 |
mtmt: | 3194164 |
Online Access: | http://publicatio.bibl.u-szeged.hu/11086 |
Tartalmi kivonat: | 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-1beta (IL-1beta) secretion in THP-1, as well as primary, human macrophages. IL-1beta secretion was dependent on NLRP3, K+-efflux, TLR4, IRAK, Syk, caspase-1, caspase-8 and NADPH-oxidase. Importantly, while C. albicans induced robust IL-1beta release after 4 h, C. parapsilosis was not able to stimulate the production of IL-1beta 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-1beta production in response to a non-albicans Candida species, and these results enhance our understanding about the immune response against C. parapsilosis. |
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Terjedelem/Fizikai jellemzők: | Terjedelem: 12 p-Azonosító: 43129 |
ISSN: | 2045-2322 |