ArticleInfection and immunity2011
Caspase-1 activation of interleukin-1β (IL-1β) and IL-18 is dispensable for induction of experimental cerebral malaria.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- A role of NLRP3 and MMP9 in migraine progression: a systematic review of translational study.Frontiers in neurology · 2024Pooled it
- Malaria-induced NLRP12/NLRP3-dependent caspase-1 activation mediates inflammation and hypersensitivity to bacterial superinfection.PLoS pathogens · 2014Trial
- Cordycepin attenuates NLRP3/Caspase-1/GSDMD-mediated LPS-induced macrophage pyroptosis.Frontiers in pharmacology · 2025Article
- Microglia exhibit a dynamic response, modulating inducible nitric oxide synthase expression and the production of pro-inflammatory cytokines during experimental cerebral malaria.Frontiers in immunology · 2025Article
- Role of inflammasomes in Toxoplasma and Plasmodium infections.Parasites & vectors · 2024Review
- Multiple sclerosis: the NLRP3 inflammasome, gasdermin D, and therapeutics.Annals of translational medicine · 2024Review
- Diversity and complexity of cell death: a historical review.Experimental & molecular medicine · 2023Review
- AIM2 sensors mediate immunity toProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Caspase-8 mediates inflammation and disease in rodent malaria.Nature communications · 2020Article
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
- Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020Review
- The Liver-StageFrontiers in immunology · 2019Article
- Inflammasome activation negatively regulates MyD88-IRF7 type I IFN signaling and anti-malaria immunity.Nature communications · 2018Article
- Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Review
- How Inflammasomes Inform Adaptive Immunity.Journal of molecular biology · 2018Review
- Host Resistance to Plasmodium-Induced Acute Immune Pathology Is Regulated by Interleukin-10 Receptor Signaling.Infection and immunity · 2017Article
- Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases.Immunological reviews · 2017Review
- IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria.PLoS pathogens · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malaria infection is initiated by sporozoite invasion of hepatocytes and asexual reproduction of liver stages, processes that are regarded to be "clinically and diagnostically silent." Merozoites, which egress from hepatocytes, infect erythrocytes in periodic cycles and induce disease. How the host innate immune system contributes to disease outcomes and to the induction of effector cells during malaria remains unclear. Likewise, how the initial liver stages may shape responses to blood-stage parasites is unknown. Here, using both sporozoite- and blood-stage-induced infections with the rodent malaria parasite Plasmodium berghei ANKA, we show that the MyD88 and Toll-like receptor 2/4 (TLR2/4) pathways play critical roles in the development of experimental cerebral malaria (ECM). Strikingly, an absolute dependence on MyD88 and TLR2/4 was observed when infections were initiated with sporozoites. In addition, we show that caspase-1 activation of interleukin-1β (IL-1β) and IL-18, which is associated with the inflammasome pathway, does not contribute to P. berghei ANKA-induced immunopathology. Consistent with these data, prophylactic cover with the IL-1β antagonist anakinra did not reduce the incidence of ECM. Therefore, we propose that protection against ECM due to loss of TLR signaling functions is caused by effector mechanisms other than IL-1β activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.