ArticlePLoS pathogens2021
Skeleton binding protein-1-mediated parasite sequestration inhibits spontaneous resolution of malaria-associated acute respiratory distress syndrome.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Differential Effects of DHA-Rich Fish Oil Supplementation on Intestinal and Pulmonary Alterations in Experimental Malaria Caused byACS omega · 2026Article
- Animal Models of Malaria-Associated Acute Kidney Injury.Seminars in nephrology · 2025Review
- Alveolar macrophages and monocyte subpopulations duringHeliyon · 2024Article
- Transcriptional responses of brain endothelium toMicrobiology spectrum · 2024Article
- Beyond the microcirculation: sequestration of infected red blood cells and reduced flow in large draining veins in experimental cerebral malaria.Nature communications · 2024Article
- Single cell RNA sequencing reveals endothelial cell killing and resolution pathways in experimental malaria-associated acute respiratory distress syndrome.PLoS pathogens · 2024Article
- A member of the tryptophan-rich protein family is required for efficient sequestration of Plasmodium berghei schizonts.PLoS pathogens · 2022Article
- Experimental Models to Study the Pathogenesis of Malaria-Associated Acute Respiratory Distress Syndrome.Frontiers in cellular and infection microbiology · 2022Review
- Experimental malaria-associated acute kidney injury is independent of parasite sequestration and resolves upon antimalarial treatment.Frontiers in cellular and infection microbiology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 RT-qPCR. 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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