ArticleEuropean journal of immunology2008
Bacillus anthracis spores and lethal toxin induce IL-1beta via functionally distinct signaling pathways.
Article in European journal of immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Toll-Like Receptors (TLRs), NOD-Like Receptors (NLRs), and RIG-I-Like Receptors (RLRs) in Innate Immunity. TLRs, NLRs, and RLRs Ligands as Immunotherapeutic Agents for Hematopoietic Diseases.International journal of molecular sciences · 2021Review
- Protein Kinase R in Bacterial Infections: Friend or Foe?Frontiers in immunology · 2021Review
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
- Clash of the Cytokine Titans: counter-regulation of interleukin-1 and type I interferon-mediated inflammatory responses.Cellular & molecular immunology · 2017Review
- Type I interferon licenses enhanced innate recognition and transcriptional responses to Franciscella tularensis live vaccine strain.Innate immunity · 2016Article
- NOD-Like Receptors in Infection, Immunity, and Diseases.Yonsei medical journal · 2016Review
- Expression of Nucleotide-oligomerization Domain (NOD) and Related Genes in Mouse Tissues Infected with Mycobacterium leprae.Immune network · 2015Article
- Regulation of the death-associated protein kinase 1 expression and autophagy via ATF6 requires apoptosis signal-regulating kinase 1.Molecular and cellular biology · 2014Article
- The IL-23/Th17 axis is involved in the adaptive immune response to Bacillus anthracis in humans.European journal of immunology · 2014Article
- An Update on PYRIN Domain-Containing Pattern Recognition Receptors: From Immunity to Pathology.Frontiers in immunology · 2013Review
- Polyacetylene Compound from Cirsium japonicum var. ussuriense Inhibited Caspase-1-mediated IL-1β Expression.Immune network · 2012Article
- Review
- Mechanisms of NK cell-macrophage Bacillus anthracis crosstalk: a balance between stimulation by spores and differential disruption by toxins.PLoS pathogens · 2012Article
- Allelic variation on murine chromosome 11 modifies host inflammatory responses and resistance to Bacillus anthracis.PLoS pathogens · 2011Article
- Inflammasomes in intestinal inflammation and cancer.Gastroenterology · 2011Review
- Targeting the inflammasome and adenosine type-3 receptors improves outcome of antibiotic therapy in murine anthrax.World journal of biological chemistry · 2011Article
- Anthrax lethal factor activates K(+) channels to induce IL-1β secretion in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Inflammasome sensor Nlrp1b-dependent resistance to anthrax is mediated by caspase-1, IL-1 signaling and neutrophil recruitment.PLoS pathogens · 2010Article
- Bacillus anthracis endospores regulate ornithine decarboxylase and inducible nitric oxide synthase through ERK1/2 and p38 mitogen-activated protein kinases.Current microbiology · 2010Article
- Proteasome inhibitors prevent caspase-1-mediated disease in rodents challenged with anthrax lethal toxin.The American journal of pathology · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Previous reports suggested that lethal toxin (LT)-induced caspase-1 activity and/or IL-1beta accounted for Bacillus anthracis (BA) infection lethality. In contrast, we now report that caspase-1-mediated IL-1beta expression in response to BA spores is required for anti-BA host defenses. Caspase-1(-/-) and IL-1beta(-/-) mice are more susceptible than wild-type (WT) mice to lethal BA infection, are less able to kill BA both in vivo and in vitro, and addition of rIL-1beta to macrophages from these mice restored killing in vitro. Non-germinating BA spores induced caspase-1 activity, IL-1beta and nitric oxide, by which BA are killed in WT but not in caspase-1(-/-) mice, suggesting that the spore itself stimulated inflammatory responses. While spores induced IL-1beta in LT-susceptible and -resistant macrophages, LT induced IL-1beta only in LT-susceptible macrophages. Cooperation between MyD88-dependent and -independent signaling pathways was required for spore-induced, but not LT-induced, IL-1beta. While both spores and LT induced caspase-1 activity and IL-1beta, LT did not induce IL-1beta mRNA, and spores did not induce cell death. Thus different components of the same bacterium each induce IL-1beta by distinct signaling pathways. Whereas the spore-induced IL-1beta limits BA infection, LT-induced IL-1beta enables BA to escape host defenses.
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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.