ArticleEuropean journal of immunology2019
Brucella abortus nitric oxide metabolite regulates inflammasome activation and IL-1β secretion in murine macrophages.
Article in European journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Host GPCR-cAMP signaling balances Gαs and Gαi activity to control intracellularbioRxiv : the preprint server for biology · 2026Article
- Brucella abortus induces dynamin-related protein 1 (DRP1)-dependent mitochondrial fission in infected macrophages via stress sensor IRE1α altering metabolic function.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Review
- Beyond survival to domination:Frontiers in microbiology · 2025Review
- ZBP1 sensesFrontiers in immunology · 2024Article
- Salmonella Enteritidis T1SS protein SiiD inhibits NLRP3 inflammasome activation via repressing the mtROS-ASC dependent pathway.PLoS pathogens · 2023Article
- Role of the cGAS/STING pathway in the control ofFrontiers in immunology · 2023Article
- Inflammatory Mechanism ofInternational journal of molecular sciences · 2022Review
- The endoplasmic reticulum stress sensor IRE1α modulates macrophage metabolic function duringFrontiers in immunology · 2022Article
- A gene expression map of host immune response in human brucellosis.Frontiers in immunology · 2022Article
- Bacterial subversion of NLR-mediated immune responses.Frontiers in immunology · 2022Review
- Galectin-3 regulates proinflammatory cytokine function and favours Brucella abortus chronic replication in macrophages and mice.Cellular microbiology · 2021Article
- STING regulates metabolic reprogramming in macrophages via HIF-1α during Brucella infection.PLoS pathogens · 2021Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
NLRP3 inflammasome is a protein complex crucial to caspase-1 activation and IL-1β and IL-18 maturation. This receptor participates in innate immune responses to different pathogens, including the bacteria of genus Brucella. Our group recently demonstrated that Brucella abortus-induced IL-1β secretion involves NLRP3 inflammasome and it is partially dependent on mitochondrial ROS production. However, other factors could be involved, such as P2X7-dependent potassium efflux, membrane destabilization, and cathepsin release. Moreover, there is increasing evidence that nitric oxide acts as a modulator of NLRP3 inflammasome. The aim of this study was to unravel the mechanism of NLRP3 inflammasome activation induced by B. abortus, as well as the involvement of bacterial nitric oxide (NO) as a modulator of this inflammasome pathway. We demonstrated that NO produced by B. abortus can be used by the bacteria to modulate IL-1β secretion in infected murine macrophages. Additionally, our results suggest that B. abortus-induced IL-1β secretion depends on a P2X7-independent potassium efflux, lysosomal acidification, cathepsin release, mechanisms clearly associated to NLRP3 inflammasome. In summary, our results help to elucidate the molecular mechanisms of NLRP3 activation and regulation during an intracellular bacterial infection.
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