期刊
PLOS PATHOGENS
卷 17, 期 11, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1010114
关键词
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资金
- L'OrealUnesco Women for Sciences PhD fellowship
- F.W.O. Vlaanderen
- Research Foundation Flanders (F.W.O. Vlaanderen) [G0C9720N]
- Research Fund (C1 project) of the KU Leuven [C16/ 17/010]
The study showed that parasite sequestration mediated by skeleton binding protein-1 (SBP-1) and high parasite load are not essential for the development of experimental malaria-associated acute respiratory distress syndrome (MA-ARDS), but inhibit the resolution of the disease.
Malaria is a hazardous disease caused by Plasmodium parasites and often results in lethal complications, including malaria-associated acute respiratory distress syndrome (MA-ARDS). Parasite sequestration in the microvasculature is often observed, but its role in malaria pathogenesis and complications is still incompletely understood. We used skeleton binding protein-1 (SBP-1) KO parasites to study the role of sequestration in experimental MA-ARDS. The sequestration-deficiency of these SBP-1 KO parasites was confirmed with bioluminescence imaging and by measuring parasite accumulation in the lungs with RTqPCR. The SBP-1 KO parasites induced similar lung pathology in the early stage of experimental MA-ARDS compared to wildtype (WT) parasites. Strikingly, the lung pathology resolved subsequently in more than 60% of the SBP-1 KO infected mice, resulting in prolonged survival despite the continuous presence of the parasite. This spontaneous disease resolution was associated with decreased inflammatory cytokine expression measured by RT-qPCR and lower expression of cytotoxic markers in pathogenic CD8(+) T cells in the lungs of SBP-1 KO infected mice. These data suggest that SBP-1-mediated parasite sequestration and subsequent high parasite load are not essential for the development of experimental MA-ARDS but inhibit the resolution of the disease.
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