ArticleNature communications2015
Inhibition of inflammasome activation by Coxiella burnetii type IV secretion system effector IcaA.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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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.
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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
61 citing papers in PubMed, 101 citations in OpenAlex.
- TGF-β/IFN-γ Antagonism in Subversion and Self-Defense of Phase II Coxiella burnetiiInfection and immunity · 2023Trial
- Beyond Acute Infection: A Conceptual Framework Linking Zoonotic Bacterial Pathogens to Pulmonary Fibrosis and Lung Carcinogenesis.Biomedicines · 2026Review
- Article
- The lipid A acylation pattern of Coxiella burnetii prevents detection and clearance by the non-canonical inflammasome in primary murine macrophages.PLoS pathogens · 2026Article
- Subverting Host Defense from Within: Innate Immune Modulation byPathogens (Basel, Switzerland) · 2026Review
- Discerning dangerous gain of function: most gain of function (GoF) research does not involve infectious microbes.Frontiers in bioengineering and biotechnology · 2026Review
- Review
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
- Modulation of host cell pathways bymLife · 2025Review
- Bacterial Puppeteering: How the Stealth BacteriumPathogens (Basel, Switzerland) · 2025Review
- CYP1B1-AS1 regulates CYP1B1 to promote Coxiella burnetii pathogenesis by inhibiting ROS and host cell death.Nature communications · 2025Article
- Coxiella burnetii as a model system for understanding host immune response against obligate intracellular, vacuolar pathogens.PLoS pathogens · 2025Article
- Identification of aInfection and immunity · 2025Article
- Article
- Caspase-8 activity mediates TNFα production and restrictsInfection and immunity · 2024Article
- Role of Type 4B Secretion System Protein, IcmE, in the Pathogenesis ofPathogens (Basel, Switzerland) · 2024Article
- Caspase-8 activity mediates TNFα production and restrictsbioRxiv : the preprint server for biology · 2024Article
- Article
- Macrophage infectivity potentiator protein, a peptidyl prolyl cis-trans isomerase, essential for Coxiella burnetii growth and pathogenesis.PLoS pathogens · 2023Article
- Resurrection of plant disease resistance proteins via helper NLR bioengineering.Science advances · 2023Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Coxiella burnetii is a highly infectious bacterium that promotes its own replication in macrophages by inhibiting several host cell responses. Here, we show that C. burnetii inhibits caspase-1 activation in primary mouse macrophages. By using co-infection experiments, we determine that the infection of macrophages with C. burnetii inhibits the caspase-11-mediated non-canonical activation of the NLRP3 inflammasome induced by subsequent infection with Escherichia coli or Legionella pneumophila. Genetic screening using flagellin mutants of L. pneumophila as a surrogate host, reveals a novel C. burnetii gene (IcaA) involved in the inhibition of caspase activation. Expression of IcaA in L. pneumophila inhibited the caspase-11 activation in macrophages. Moreover, icaA(-) mutants of C. burnetii failed to suppress the caspase-11-mediated inflammasome activation induced by L. pneumophila. Our data reveal IcaA as a novel C. burnetii effector protein that is secreted by the Dot/Icm type IV secretion system and interferes with the caspase-11-induced, non-canonical activation of the inflammasome.
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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.