期刊
FRONTIERS IN IMMUNOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2020.565869
关键词
whole blood ex vivo model; host-pathogen interaction; Candida albicans; neutrophils; mice
类别
资金
- funding line Strategic Networking in the Leibniz Association
- FWF Austrian Science Fund [P26117-B20]
- German Research Foundation (DFG) [TRR 124, 210879364]
- Austrian Science Fund (FWF) [P26117] Funding Source: Austrian Science Fund (FWF)
By adapting the human whole-blood model to murine blood, it was found that murine blood has a weaker ability to reduce fungal burden and control filamentation of C. albicans compared to human blood. The lower neutrophil count in murine blood partially explains the insufficient infection control, and differences in host-pathogen interactions were observed, particularly in platelet interactions with C. albicans.
Murine infection models are widely used to study systemic candidiasis caused by C. albicans. Whole-blood models can help to elucidate host-pathogens interactions and have been used for several Candida species in human blood. We adapted the human whole-blood model to murine blood. Unlike human blood, murine blood was unable to reduce fungal burden and more substantial filamentation of C. albicans was observed. This coincided with less fungal association with leukocytes, especially neutrophils. The lower neutrophil number in murine blood only partially explains insufficient infection and filamentation control, as spiking with murine neutrophils had only limited effects on fungal killing. Furthermore, increased fungal survival is not mediated by enhanced filamentation, as a filament-deficient mutant was likewise not eliminated. We also observed host-dependent differences for interaction of platelets with C. albicans, showing enhanced platelet aggregation, adhesion and activation in murine blood. For human blood, opsonization was shown to decrease platelet interaction suggesting that complement factors interfere with fungus-to-platelet binding. Our results reveal substantial differences between murine and human whole-blood models infected with C. albicans and thereby demonstrate limitations in the translatability of this ex vivo model between hosts.
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