ArticlePLoS neglected tropical diseases2013
NLRP3 controls Trypanosoma cruzi infection through a caspase-1-dependent IL-1R-independent NO production.
Article in PLoS neglected tropical diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
68 citing papers in PubMed, 119 citations in OpenAlex.
- Review
- Chagas disease: host responses, parasite evasion and vaccine advances.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2026Review
- Placental immunopathology and congenital transmission of Zika virus andFrontiers in immunology · 2026Review
- The P2X7 Receptor and Its Relation to Neglected Tropical Diseases: Focusing on Chagas Disease.Journal of tropical medicine · 2026Review
- Immunological and inflammatory responses in the kidneys in experimental acanthamoebiasis.Microbiology spectrum · 2025Article
- Mitochondrial damage and IL-1β production in monocytes caused byFrontiers in immunology · 2025Article
- NOD-like receptors in fish: evolution, structure, immune signaling, and targeting for aquaculture vaccine adjuvants.Frontiers in immunology · 2025Review
- Molecular regulation of NLRP3 inflammasome activation during parasitic infection.Bioscience reports · 2024Review
- Roles of ADP-Ribosylation during Infection Establishment byPathogens (Basel, Switzerland) · 2023Review
- Effect and mechanism of reactive oxygen species-mediated NOD-like receptor family pyrin domain-containing 3 inflammasome activation in hepatic alveolar echinococcosis.World journal of gastroenterology · 2023Article
- Cell type-specific roles of NLRP3, inflammasome-dependent and -independent, in host defense, sterile necroinflammation, tissue repair, and fibrosis.Frontiers in immunology · 2023Review
- NAIP/NLRC4 inflammasome participates in macrophage responses toFrontiers in immunology · 2023Article
- Age and Chronodisruption in Mouse Heart: Effect of the NLRP3 Inflammasome and Melatonin Therapy.International journal of molecular sciences · 2022Article
- IFN-induced cell-autonomous immune mechanisms in the control of intracellular protozoa.Parasitology research · 2022Review
- Sheltered in Stromal Tissue Cells,Pathogens (Basel, Switzerland) · 2022Article
- IL-1β is not critical to chronic heart dysfunction in mice with Chagas disease.Frontiers in immunology · 2022Article
- Gasdermins in Innate Host Defense AgainstFrontiers in immunology · 2022Review
- Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections.International journal of molecular sciences · 2021Review
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Virulence ofFrontiers in cellular and infection microbiology · 2021Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trypanosoma cruzi (T. cruzi) is an intracellular protozoan parasite and the etiological agent of Chagas disease, a chronic infectious illness that affects millions of people worldwide. Although the role of TLR and Nod1 in the control of T. cruzi infection is well-established, the involvement of inflammasomes remains to be elucidated. Herein, we demonstrate for the first time that T. cruzi infection induces IL-1β production in an NLRP3- and caspase-1-dependent manner. Cathepsin B appears to be required for NLRP3 activation in response to infection with T. cruzi, as pharmacological inhibition of cathepsin B abrogates IL-1β secretion. NLRP3(-/-) and caspase1(-/-) mice exhibited high numbers of T. cruzi parasites, with a magnitude of peak parasitemia comparable to MyD88(-/-) and iNOS(-/-) mice (which are susceptible models for T. cruzi infection), indicating the involvement of NLRP3 inflammasome in the control of the acute phase of T. cruzi infection. Although the inflammatory cytokines IL-6 and IFN-γ were found in spleen cells from NLRP3(-/-) and caspase1(-/-) mice infected with T. cruzi, these mice exhibited severe defects in nitric oxide (NO) production and an impairment in macrophage-mediated parasite killing. Interestingly, neutralization of IL-1β and IL-18, and IL-1R genetic deficiency demonstrate that these cytokines have a minor effect on NO secretion and the capacity of macrophages to control T. cruzi infection. In contrast, inhibition of caspase-1 with z-YVAD-fmk abrogated NO production by WT and MyD88(-/-) macrophages and rendered them as susceptible to T. cruzi infection as NLRP3(-/-) and caspase-1(-/-) macrophages. Taken together, our results demonstrate a role for the NLRP3 inflammasome in the control of T. cruzi infection and identify NLRP3-mediated, caspase-1-dependent and IL-1R-independent NO production as a novel effector mechanism for these innate receptors.
Indexed as
Identifiers
What OpenQuestion holds
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.