ArticleMediators of inflammation2016
Caspase-11 Modulates Inflammation and Attenuates Toxoplasma gondii Pathogenesis.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Insight Into Inflammasome Signaling: Implications forFrontiers in immunology · 2020Pooled it
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Mitochondrial damage and IL-1β production in monocytes caused byFrontiers in immunology · 2025Article
- Role of inflammasomes in Toxoplasma and Plasmodium infections.Parasites & vectors · 2024Review
- Pathophysiology and mechanisms of hearing impairment related to neonatal infection diseases.Frontiers in microbiology · 2023Review
- Article
- Seroprevalence and Genetic Characterization ofJournal of tropical medicine · 2022Article
- RIPK3 Facilitates Host Resistance to Oral Toxoplasma gondii Infection.Infection and immunity · 2021Article
- TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection.Parasites & vectors · 2020Article
- Gasdermin-D-dependent IL-1α release from microglia promotes protective immunity during chronic Toxoplasma gondii infection.Nature communications · 2020Article
- The molecular biology and immune control of chronic Toxoplasma gondii infection.The Journal of clinical investigation · 2020Review
- IL-1R Regulates Disease Tolerance and Cachexia inJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
- Interplay Between Reactive Oxygen Species and the Inflammasome Are Crucial for Restriction ofFrontiers in cellular and infection microbiology · 2020Article
- Immunocompetent host develops mild intestinal inflammation in acute infection with Toxoplasma gondii.PloS one · 2018Article
- NLRP3 Inflammasome Participates in Host Response toFrontiers in immunology · 2018Article
- Toxoplasma genotyping in congenital toxoplasmosis in Upper Egypt: evidence of type I strain.Parasitology research · 2017Article
- Inflammasomes and intestinal inflammation.Mucosal immunology · 2017Review
- Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases.Immunological reviews · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Toxoplasma gondii is an obligate intracellular parasite that is the etiologic agent responsible for toxoplasmosis. Infection with T. gondii results in activation of nucleotide binding domain and leucine rich repeat containing receptors (NLRs). NLR activation leads to inflammasome formation, the activation of caspase-1, and the subsequent cleavage of IL-1β and IL-18. Recently, a noncanonical inflammasome has been characterized which functions through caspase-11 and appears to augment many biological functions previously considered to be dependent upon the canonical inflammasome. To better elucidate the function of this noncanonical inflammasome in toxoplasmosis, we utilized Asc (-/-) and Casp11 (-/-) mice and infected these animals with T. gondii. Our data indicates that caspase-11 modulates the innate immune response to T. gondii through a mechanism which is distinct from that currently described for the canonical inflammasome. Asc (-/-) mice demonstrated increased disease pathogenesis during the acute phase of T. gondii infection, whereas Casp11 (-/-) mice demonstrated significantly attenuated disease pathogenesis and reduced inflammation. This attenuated host response was associated with reduced local and systemic cytokine production, including diminished IL-1β. During the chronic phase of infection, caspase-11 deficiency resulted in increased neuroinflammation and tissue cyst burden in the brain. Together, our data suggest that caspase-11 functions to protect the host by enhancing inflammation during the early phase of infection in an effort to minimize disease pathogenesis during later stages of toxoplasmosis.
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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.