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Single cell RNA sequencing reveals endothelial cell killing and resolution pathways in experimental malaria-associated acute respiratory distress syndrome. | LitMetric

AI Article Synopsis

  • Plasmodium parasites cause malaria, leading to over 200 million cases and 600,000 deaths annually, with complications like malaria-associated acute respiratory distress syndrome (MA-ARDS) contributing significantly to mortality despite effective antimalarial drugs.* -
  • A study on infected mice showed that treatment with antimalarial drugs post-symptom onset resulted in 80% survival, while alterations in lung function and inflammation were observed during infection and recovery.* -
  • The research highlights important changes in inflammatory pathways and endothelial cell behavior during the resolution phase of MA-ARDS, suggesting potential new therapeutic strategies to enhance recovery after parasite elimination.*

Article Abstract

Plasmodium parasites cause malaria, a global health disease that is responsible for more than 200 million clinical cases and 600 000 deaths each year. Most deaths are caused by various complications, including malaria-associated acute respiratory distress syndrome (MA-ARDS). Despite the very rapid and efficient killing of parasites with antimalarial drugs, 15% of patients with complicated malaria succumb. This stresses the importance of investigating resolution mechanisms that are involved in the recovery from these complications once the parasite is killed. To study the resolution of MA-ARDS, P. berghei NK65-infected C57BL/6 mice were treated with antimalarial drugs after onset of symptoms, resulting in 80% survival. Micro-computed tomography revealed alterations of the lungs upon infection, with an increase in total and non-aerated lung volume due to edema. Whole body plethysmography confirmed a drastically altered lung ventilation, which was restored during resolution. Single-cell RNA sequencing indicated an increased inflammatory state in the lungs upon infection, which was accompanied by a drastic decrease in endothelial cells, consistent with CD8+ T cell-mediated killing. During resolution, anti-inflammatory pathways were upregulated and proliferation of endothelial cells was observed. MultiNicheNet interactome analysis identified important changes in the ligand-receptor interactions during disease resolution that warrant further exploration in order to develop new therapeutic strategies. In conclusion, our study provides insights in pro-resolving pathways that limit inflammation and promote endothelial cell proliferation in experimental MA-ARDS. This information may be useful for the design of adjunctive treatments to enhance resolution after Plasmodium parasite killing by antimalarial drugs.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10826972PMC
http://dx.doi.org/10.1371/journal.ppat.1011929DOI Listing

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