ArticleThe Journal of infectious diseases2016
Human C1-Inhibitor Suppresses Malaria Parasite Invasion and Cytoadhesion via Binding to Parasite Glycosylphosphatidylinositol and Host Cell Receptors.
Article in The Journal of infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Protective Vaccination of Mice Against Blood-Stage Malaria Impacts Hepatic Expression of Genes Encoding Acute-Phase Proteins and IL-6 Family Members.International journal of molecular sciences · 2025Article
- Deceiving and escaping complement - the evasive journey of the malaria parasite.Trends in parasitology · 2022Review
- The Defensive Interactions of Prominent Infectious Protozoan Parasites: The Host's Complement System.Biomolecules · 2022Review
- Hijacking the human complement inhibitor C4b-binding protein by the sporozoite stage of theFrontiers in immunology · 2022Article
- Vector saliva controlled inflammatory response of the host may represent the Achilles heel during pathogen transmission.The journal of venomous animals and toxins including tropical diseases · 2021Article
- Complement in malaria: immune evasion strategies and role in protective immunity.FEBS letters · 2020Review
- Haem oxygenase protects against thrombocytopaenia and malaria-associated lung injury.Malaria journal · 2020Article
- Viral Evasion of the Complement System and Its Importance for Vaccines and Therapeutics.Frontiers in immunology · 2020Review
- Innate immunity to malaria-The role of monocytes.Immunological reviews · 2020Review
- The core genes involved in the promotion of depression in patients with ovarian cancer.Oncology letters · 2019Article
- Myxozoan Adhesion and Virulence:Microorganisms · 2019Article
- Complement Evasion: An Effective Strategy That Parasites Utilize to Survive in the Host.Frontiers in microbiology · 2019Review
- Signaling Strategies of Malaria Parasite for Its Survival, Proliferation, and Infection during Erythrocytic Stage.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Plasmodium falciparum-induced severe malaria remains a continuing problem in areas of endemicity, with elevated morbidity and mortality. Drugs targeting mechanisms involved in severe malaria pathology, including cytoadhesion of infected red blood cells (RBCs) to host receptors and production of proinflammatory cytokines, are still necessary. Human C1-inhibitor (C1INH) is a multifunctional protease inhibitor that regulates coagulation, vascular permeability, and inflammation, with beneficial effects in inflammatory disease models, including septic shock. We found that human C1INH, at therapeutically relevant doses, blocks severe malaria pathogenic processes by 2 distinct mechanisms. First, C1INH bound to glycan moieties within P. falciparum glycosylphosphatidylinositol (PfGPI) molecules on the parasite surface, inhibiting parasite RBC invasion and proinflammatory cytokine production by parasite-stimulated monocytes in vitro and reducing parasitemia in a rodent model of experimental cerebral malaria (ECM) in vivo. Second, C1INH bound to host CD36 and chondroitin sulfate A molecules, interfering with cytoadhesion of infected RBCs by competitive binding to these receptors in vitro and reducing sequestration in specific tissues and protecting against ECM in vivo. This study reveals that C1INH is a potential therapeutic antimalarial molecule able to interfere with severe-disease etiology at multiple levels through specific interactions with both parasite PfGPIs and host cell receptors.
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Registered trials
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