ArticleBioMed research international2014
Reduction of experimental cerebral malaria and its related proinflammatory responses by the novel liposome-based β-methasone nanodrug.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Hormones in malaria infection: influence on disease severity, host physiology, and therapeutic opportunities.Bioscience reports · 2024Review
- Administration of rIL-33 Restores Altered mDC/pDC Ratio, MDSC Frequency, and Th-17/Treg Ratio during Experimental Cerebral Malaria.Pathogens (Basel, Switzerland) · 2024Article
- Current trends and future perspectives of stroke management through integrating health care team and nanodrug delivery strategy.Frontiers in cellular neuroscience · 2023Review
- Liposomes for malaria management: the evolution from 1980 to 2020.Malaria journal · 2021Review
- Nanotechnological strategies for systemic microbial infections treatment: A review.International journal of pharmaceutics · 2020Review
- Characterization of Plasmodium berghei Homologues of T-cell Immunomodulatory Protein as a New Potential Candidate for Protecting against Experimental Cerebral Malaria.The Korean journal of parasitology · 2019Article
- The Glycosylphosphatidylinositol Transamidase Complex Subunit PbGPI16 of Plasmodium berghei Is Important for Inducing Experimental Cerebral Malaria.Infection and immunity · 2018Article
- The Multirole of Liposomes in Therapy and Prevention of Infectious Diseases.Frontiers in immunology · 2018Review
- Indocyanine Green Liposomes for Diagnosis and Therapeutic Monitoring of Cerebral Malaria.Theranostics · 2016Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral malaria (CM) is a severe complication of and a leading cause of death due to Plasmodium falciparum infection. CM is likely the result of interrelated events, including mechanical obstruction due to parasite sequestration in the microvasculature, and upregulation of Th1 immune responses. In parallel, blood-brain-barrier (BBB) breakdown and damage or death of microglia, astrocytes, and neurons occurs. We found that a novel formulation of a liposome-encapsulated glucocorticosteroid, β-methasone hemisuccinate (nSSL-BMS), prevents experimental cerebral malaria (ECM) in a murine model and creates a survival time-window, enabling administration of an antiplasmodial drug before severe anemia develops. nSSL-BMS treatment leads to lower levels of cerebral inflammation, expressed by altered levels of corresponding cytokines and chemokines. The results indicate the role of integrated immune responses in ECM induction and show that the new steroidal nanodrug nSSL-BMS reverses the balance between the Th1 and Th2 responses in malaria-infected mice so that the proinflammatory processes leading to ECM are prevented. Overall, because of the immunopathological nature of CM, combined immunomodulator/antiplasmodial treatment should be considered for prevention/treatment of human CM and long-term cognitive damage.
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