ArticleMalaria journal2015
A potential role for interleukin-33 and γ-epithelium sodium channel in the pathogenesis of human malaria associated lung injury.
Article in Malaria journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Hemozoin induces neuronal injury primarily characterized by axon rupture and mitochondrial damage in experimental cerebral malaria.Parasites & vectors · 2025Article
- Neutrophil activation, acute lung injury and disease severity in Plasmodium knowlesi malaria.PLoS neglected tropical diseases · 2024Article
- Apoptotic changes and aquaporin-1 expression in the choroid plexus of cerebral malaria patients.Malaria journal · 2022Article
- Experimental Models to Study the Pathogenesis of Malaria-Associated Acute Respiratory Distress Syndrome.Frontiers in cellular and infection microbiology · 2022Review
- Streptozotocin induces alpha-2u globulin nephropathy in male rats during diabetic kidney disease.BMC veterinary research · 2021Article
- Evaluating the effect of rice (Oryza sativa L.: SRNC05053-6-2) crude extract on psoriasis using in vitro and in vivo models.Scientific reports · 2020Article
- Case Report: The First Direct Evidence ofThe American journal of tropical medicine and hygiene · 2020Article
- The IL-33/ST2 Axis in Immune Responses Against Parasitic Disease: Potential Therapeutic Applications.Frontiers in cellular and infection microbiology · 2020Review
- Endothelial Protein C Receptor Could Contribute to Experimental Malaria-Associated Acute Respiratory Distress Syndrome.Journal of immunology research · 2019Article
- Featured Article: Immunomodulatory effect of hemozoin on pneumocyte apoptosis via CARD9 pathway, a possibly retarding pulmonary resolution.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- The Rough Guide to Monocytes in Malaria Infection.Frontiers in immunology · 2018Review
- Neutrophils and Malaria.Frontiers in immunology · 2018Review
- EPCR and Malaria Severity: The Center of a Perfect Storm.Trends in parasitology · 2017Review
- Article
- Targeting Neutrophils to Prevent Malaria-Associated Acute Lung Injury/Acute Respiratory Distress Syndrome in Mice.PLoS pathogens · 2016Article
- IL-33 Signaling in Lung Injury.Translational perioperative and pain medicine · 2016Article
- Altered Lipid Composition of Surfactant and Lung Tissue in Murine Experimental Malaria-Associated Acute Respiratory Distress Syndrome.PloS one · 2015Article
- Interleukin-33 and its Receptor in Pulmonary Inflammatory Diseases.Critical reviews in immunology · 2015Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe pathogenesis of pulmonary oedema (PE) in patients with severe malaria is still unclear. It has been hypothesized that lung injury depends, in addition to microvascular obstruction, on an increased pulmonary capillary pressure and altered alveolar-capillary membrane permeability, causing pulmonary fluid accumulation.
methodsThis study compared the histopathological features of lung injury in Southeast Asian patients (n = 43) who died from severe Plasmodium falciparum malaria, and correlated these with clinical history in groups with or without PE. To investigate the expression of mediators that may influence fluid accumulation in PE, immunohistochemistry and image analysis were performed on controls and sub-sets of patient with or without PE.
resultsThe expression of leukocyte sub-set antigens, bronchial interleukin (IL)-33, γ-epithelium sodium channel (ENaC), aquaporin (AQP)-1 and -5, and control cytokeratin staining was quantified in the lung tissue of severe malaria patients. Bronchial IL-33 expression was significantly increased in severe malaria patients with PE. Malaria patients with shock showed significantly increased bronchial IL-33 compare to other clinical manifestations. Bronchial IL-33 levels were positively correlated with CD68+ monocyte and elastase + neutrophil, septal congestion and hyaline membrane formation. Moreover, the expression of both vascular smooth muscle cell (VSMC) and bronchial γ-ENaC significantly decreased in severe malaria patients with PE. Both VSMC and bronchial γ-ENaC were negatively correlated with the degree of parasitized erythrocyte sequestration, alveolar thickness, alveolar expansion score, septal congestion score, and malarial pigment score. In contrast AQP-1 and -5 and pan cytokeratin levels were similar between groups.
conclusionsThe results suggest that IL-33 may play a role in lung injury during severe malaria and lead to PE. Both VSMC and bronchial γ-ENaC downregulation may explain pulmonary fluid disturbances and participate in PE pathogenesis in severe malaria patients.
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