ReviewSeminars in immunopathology2017
The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection.
Review in Seminars in immunopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.
- The research trend on neurobrucellosis over the past 30 years (1993-2023): a bibliometric and visualization analysis.Frontiers in neurology · 2024Pooled it
- Insight Into Inflammasome Signaling: Implications forFrontiers in immunology · 2020Pooled it
- GBP5-triggered AIM2 inflammasome drives host defense and exacerbates disease severity during Neospora caninum infection.Veterinary research · 2026Article
- The impact of STING signaling on myeloid cells highlights macrophages as the major player in controllingFrontiers in immunology · 2025Article
- Review
- Review
- Inflammasomes and idiopathic inflammatory myopathies.Frontiers in immunology · 2024Review
- Expression of NLRP3 and AIM2 inflammasome in Peripheral blood in Chinese patients with acute and chronic brucellosis.Scientific reports · 2022Article
- Glial Cells and Brain Diseases: Inflammasomes as Relevant Pathological Entities.Frontiers in cellular neuroscience · 2022Review
- Galectin-3 regulates proinflammatory cytokine function and favours Brucella abortus chronic replication in macrophages and mice.Cellular microbiology · 2021Article
- Microglia Biomarkers in Alzheimer's Disease.Molecular neurobiology · 2021Review
- Host Immune Responses and Pathogenesis toPathogens (Basel, Switzerland) · 2021Article
- Uncovering the Hidden Credentials ofMicrobiology and molecular biology reviews : MMBR · 2021Review
- NLRP6-associated host microbiota composition impacts in the intestinal barrier to systemic dissemination of Brucella abortus.PLoS neglected tropical diseases · 2021Article
- Doxycycline Induces Apoptosis ofFrontiers in cellular and infection microbiology · 2021Article
- By Regulating the NLRP3 Inflammasome Can Reduce the Release of Inflammatory Factors in the Co-Culture Model of Tuberculosis H37Ra Strain and Rat Microglia.Frontiers in cellular and infection microbiology · 2021Article
- ASC-Mediated Inflammation and Pyroptosis AttenuatesPathogens (Basel, Switzerland) · 2020Article
- Immunological pathways of macrophage response toInnate immunity · 2020Article
- Inflammasome and Mitophagy Connection in Health and Disease.International journal of molecular sciences · 2020Review
- Characterization of the NLRP1 inflammasome response in bovine species.Innate immunity · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The innate immune system is essential for the detection and elimination of bacterial pathogens. Upon inflammasome activation, caspase-1 cleaves pro-IL-1β and pro-IL-18 to their mature forms IL-1β and IL-18, respectively, and the cell undergoes inflammatory death termed pyroptosis. Here, we reviewed recent findings demonstrating that Brucella abortus ligands activate NLRP3 and AIM2 inflammasomes which lead to control of infection. This protective effect is due to the inflammatory response caused by IL-1β and IL-18 rather than cell death. Brucella DNA is sensed by AIM2 and bacteria-induced mitochondrial reactive oxygen species is detected by NLRP3. However, deregulation of pro-inflammatory cytokine production can lead to immunopathology. Nervous system invasion by bacteria of the genus Brucella results in an inflammatory disorder termed neurobrucellosis. Herein, we discuss the mechanism of caspase-1 activation and IL-1β secretion in glial cells infected with B. abortus. Our results demonstrate that the ASC inflammasome is indispensable for inducing the activation of caspase-1 and secretion of IL-1β upon infection of astrocytes and microglia with Brucella. Moreover, our results demonstrate that secretion of IL-1β by Brucella-infected glial cells depends on NLRP3 and AIM2 and leads to neurobrucellosis. Further, the inhibition of the host cell inflammasome as an immune evasion strategy has been described for bacterial pathogens. We discuss here that the bacterial type IV secretion system VirB is required for inflammasome activation in host cells during infection. Taken together, our results indicate that Brucella is sensed by ASC inflammasomes mainly NLRP3 and AIM2 that collectively orchestrate a robust caspase-1 activation and pro-inflammatory response.
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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.