ArticlePLoS pathogens2019
Non-canonical NLRP3 inflammasome activation and IL-1β signaling are necessary to L. amazonensis control mediated by P2X7 receptor and leukotriene B4.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Lipid Mediators in Host-Pathogen Interactions duringACS infectious diseases · 2026Review
- The P2X7 Receptor and Its Relation to Neglected Tropical Diseases: Focusing on Chagas Disease.Journal of tropical medicine · 2026Review
- Article
- New insights into the noncanonical inflammasome point to caspase-4 as a druggable target.Nature reviews. Immunology · 2025Review
- Activation Pathways of Murine Macrophages by Lipophosphoglycan from Strains ofACS infectious diseases · 2024Article
- NLRP1-dependent activation of Gasdermin D in neutrophils controls cutaneous leishmaniasis.PLoS pathogens · 2024Article
- Molecular regulation of NLRP3 inflammasome activation during parasitic infection.Bioscience reports · 2024Review
- P2X7 receptor inhibition alleviates mania-like behavior independently of interleukin-1β.iScience · 2024Article
- Gasdermin-D activation promotes NLRP3 activation and host resistance to Leishmania infection.Nature communications · 2023Article
- Leukotrienes in Innate Immunity: Still Underappreciated after All These Years?Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Activated P2X receptors can up-regulate the expressions of inflammation-related genes via NF-κB pathway in spotted sea bass (Frontiers in immunology · 2023Article
- Cysteinyl-leukotrienes promote cutaneous Leishmaniasis control.Frontiers in cellular and infection microbiology · 2023Article
- Repurposing the Antibacterial Agents Peptide 19-4LF and Peptide 19-2.5 for Treatment of Cutaneous Leishmaniasis.Pharmaceutics · 2022Article
- Toxoplasma gondii Infection Decreases Intestinal 5-Lipoxygenase Expression, while Exogenous LTBInfection and immunity · 2022Article
- Purinergic modulation of the immune response to infections.Purinergic signalling · 2022Review
- Purinergic signaling: A new front-line determinant of resistance and susceptibility in leishmaniasis.Biomedical journal · 2022Review
- Exploring the Use of Medicinal Plants and Their Bioactive Derivatives as Alveolar NLRP3 Inflammasome Regulators duringInternational journal of molecular sciences · 2021Review
- Review
- Leukotriene BBiomedicines · 2021Article
- Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.Immunological reviews · 2021Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leishmaniasis is a neglected tropical disease affecting millions of individuals worldwide. P2X7 receptor has been linked to the elimination of Leishmania amazonensis. Biological responses evoked by P2X7 receptor activation have been well-documented, including apoptosis, phagocytosis, cytokine release, such as IL-1β. It was demonstrated that NLRP3 inflammasome activation and IL-1β signaling participated in resistance against L. amazonensis. Furthermore, our group has shown that L. amazonensis elimination through P2X7 receptor activation depended on leukotriene B4 (LTB4) production and release. Therefore, we investigated whether L. amazonensis elimination by P2X7 receptor and LTB4 involved NLRP3 inflammasome activation and IL-1β signaling. We showed that macrophages from NLRP3-/-, ASC-/-, Casp-1/11-/-, gp91phox-/- , and IL-1R-/- mice treated with ATP or LTB4 did not decrease parasitic load as was observed in WT mice. When ASC-/- macrophages were treated with exogenous IL-1β, parasite killing was noted, however, we did not see parasitic load reduction in IL-1R-/- macrophages. Similarly, macrophages from P2X7 receptor-deficient mice treated with IL-1β also showed decreased parasitic load. In addition, when we infected Casp-11-/- macrophages, neither ATP nor LTB4 were able to reduce parasitic load, and Casp-11-/- mice were more susceptible to L. amazonensis infection than were WT mice. Furthermore, P2X7-/- L. amazonensis-infected mice locally treated with exogenous LTB4 showed resistance to infection, characterized by lower parasite load and smaller lesions compared to untreated P2X7-/- mice. A similar observation was noted when infected P2X7-/- mice were treated with IL-1β, i.e., lower parasite load and smaller lesions compared to P2X7-/- mice. These data suggested that L. amazonensis elimination mediated by P2X7 receptor and LTB4 was dependent on non-canonical NLRP3 inflammasome activation, ROS production, and IL-1β signaling.
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