ArticleThe Journal of biological chemistry2011
Apoptosis-associated speck-like protein (ASC) controls Legionella pneumophila infection in human monocytes.
Article in The Journal of biological chemistry, 2011. 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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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
34 citing papers in PubMed, 60 citations in OpenAlex.
- Pyroptosis: Molecular mechanisms and function.Journal of physiology and biochemistry · 2026Review
- Uncoupled pyroptosis and IL-1β secretion downstream of inflammasome signaling.Frontiers in immunology · 2023Review
- Insights into inflammasome regulation: cellular, molecular, and pathogenic control of inflammasome activation.Immunologic research · 2022Review
- Human Amnion Epithelial Cells (AECs) Respond to the FSL-1 Lipopeptide by Engaging the NLRP7 Inflammasome.Frontiers in immunology · 2020Article
- Methylomic correlates of autophagy activity in cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2019Article
- Brucella abortus nitric oxide metabolite regulates inflammasome activation and IL-1β secretion in murine macrophages.European journal of immunology · 2019Article
- Emerging Roles of Autophagy and Inflammasome in Ehrlichiosis.Frontiers in immunology · 2019Review
- Inhibition of caspase-1 or gasdermin-D enable caspase-8 activation in the Naip5/NLRC4/ASC inflammasome.PLoS pathogens · 2017Article
- Caspase Exploitation by Legionella pneumophila.Frontiers in microbiology · 2016Review
- Caspase-11 and caspase-1 differentially modulate actin polymerization via RhoA and Slingshot proteins to promote bacterial clearance.Scientific reports · 2015Article
- Human caspase-4 and caspase-5 regulate the one-step non-canonical inflammasome activation in monocytes.Nature communications · 2015Article
- The cooperation between the autophagy machinery and the inflammasome to implement an appropriate innate immune response: do they regulate each other?Immunological reviews · 2015Review
- Complete and ubiquitinated proteome of the Legionella-containing vacuole within human macrophages.Journal of proteome research · 2015Article
- Article
- Inflammasome-mediated cell death in response to bacterial pathogens that access the host cell cytosol: lessons from legionella pneumophila.Frontiers in cellular and infection microbiology · 2013Review
- NLRP3 inflammasome and host protection against bacterial infection.Journal of Korean medical science · 2013Review
- Haemophilus ducreyi infection induces activation of the NLRP3 inflammasome in nonpolarized but not in polarized human macrophages.Infection and immunity · 2013Article
- Review
- A bacterial protein promotes the recognition of the Legionella pneumophila vacuole by autophagy.European journal of immunology · 2013Article
- Biofilm-derived Legionella pneumophila evades the innate immune response in macrophages.Frontiers in cellular and infection microbiology · 2013Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
The ability of Legionella pneumophila to cause pneumonia is determined by its capability to evade the immune system and grow within human monocytes and their derived macrophages. Human monocytes efficiently activate caspase-1 in response to Salmonella but not to L. pneumophila. The molecular mechanism for the lack of inflammasome activation during L. pneumophila infection is unknown. Evaluation of the expression of several inflammasome components in human monocytes during L. pneumophila infection revealed that the expression of the apoptosis-associated speck-like protein (ASC) and the NOD-like receptor NLRC4 are significantly down-regulated in human monocytes. Exogenous expression of ASC maintained the protein level constant during L. pneumophila infection and conveyed caspase-1 activation and restricted the growth of the pathogen. Further depletion of ASC with siRNA was accompanied with improved NF-κB activation and enhanced L. pneumophila growth. Therefore, our data demonstrate that L. pneumophila manipulates ASC levels to evade inflammasome activation and grow in human monocytes. By targeting ASC, L. pneumophila modulates the inflammasome, the apoptosome, and NF-κB pathway simultaneously.
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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.