ArticleMalaria journal2020
Haem oxygenase protects against thrombocytopaenia and malaria-associated lung injury.
Article in Malaria journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Beyond the mouse: organoids, spheroids, and organs-on-chips as the (inevitable) future of malaria research?Malaria journal · 2026Review
- Plasmodium yoelii infection induces lung injury by modulating type 2 conventional dendritic cells autophagy via the STAT3-IRF4 signaling.Cell death & disease · 2026Article
- Differential Effects of DHA-Rich Fish Oil Supplementation on Intestinal and Pulmonary Alterations in Experimental Malaria Caused byACS omega · 2026Article
- Heme and hemozoin induce platelet cell death through UPR-induced apoptosis and ferroptosis in vivax malaria.Blood advances · 2026Article
- Heme oxygenase-1 and malaria pathogenesis.Frontiers in immunology · 2026Review
- Article
- Experimental Models to Study the Pathogenesis of Malaria-Associated Acute Respiratory Distress Syndrome.Frontiers in cellular and infection microbiology · 2022Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundMalaria-triggered lung injury can occur in both severe and non-severe cases. Platelets may interact with parasitized erythrocytes, leukocytes and endothelium. These interactions can lead to microvessel obstructions and induce release of inflammatory mediators. Induction of the haem oxygenase enzyme is important in the host's response to free haem and to several other molecules generated by infectious or non-infectious diseases. In addition, an important role for the haem oxygenase-1 isotype has been demonstrated in experimental cerebral malaria and in clinical cases. Therefore, the present work aims to determine the influence of haem oxygenase in thrombocytopaenia and acute pulmonary injury during infection with Plasmodium berghei strain NK65.
methodsC57BL/6 mice were infected with P. berghei and analysed 7-10 days post-infection. For each experiment, Cobalt Protoporphyrin IX/CoPPIX or saline were administered. Bronchoalveolar lavage fluid was used for total and differential leukocyte count and for protein measurement. Lungs were used for histological analyses or for analysis of cytokines and western blotting. The lung permeability was analysed by Evans blue dye concentration. Platelet-leukocyte aggregate formation was assayed using the flow cytometer.
resultsPlasmodium berghei NK65 infection generated an intense lung injury, with increased levels of inflammatory mediators, oedema, and cell migration into the lung. Plasmodium berghei infection was also accompanied by marked thrombocytopaenia and formation of platelet-leukocyte aggregates in peripheral blood. Treatment with the HO-1 inducer cobalt protoporphyrin IX (CoPPIX) modified the inflammatory response but did not affect the evolution of parasitaemia. Animals treated with CoPPIX showed an improvement in lung injury, with decreased inflammatory infiltrate in the lung parenchyma, oedema and reduced thrombocytopaenia.
conclusionData here presented suggest that treatment with CoPPIX inducer leads to less severe pulmonary lung injury and thrombocytopaenia during malaria infection, thus increasing animal survival.
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