ArticlePloS one2015
Inflammasome priming is similar for francisella species that differentially induce inflammasome activation.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
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- cAbl Kinase Regulates Inflammasome Activation and Pyroptosis via ASC Phosphorylation.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.Microbiology and molecular biology reviews : MMBR · 2021Review
- Checks and Balances between Autophagy and Inflammasomes during Infection.Journal of molecular biology · 2018Review
- Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein DuringFrontiers in immunology · 2018Article
- Complement C3 as a Prompt for Human Macrophage Death during Infection with Francisella tularensis Strain SCHU S4.Infection and immunity · 2017Article
- Article
- Bacterial secretion systems and regulation of inflammasome activation.Journal of leukocyte biology · 2017Review
- Mitogen-activated protein kinases (MAPKs) are modulated during Francisella tularensis infection, but inhibition of extracellular-signal-regulated kinases (ERKs) is of limited therapeutic benefit.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Inflammasome activation is a two-step process where step one, priming, prepares the inflammasome for its subsequent activation, by step two. Classically step one can be induced by LPS priming followed by step two, high dose ATP. Furthermore, when IL-18 processing is used as the inflammasome readout, priming occurs before new protein synthesis. In this context, how intracellular pathogens such as Francisella activate the inflammasome is incompletely understood, particularly regarding the relative importance of priming versus activation steps. To better understand these events we compared Francisella strains that differ in virulence and ability to induce inflammasome activation for their relative effects on step one vs. step two. When using the rapid priming model, i.e., 30 min priming by live or heat killed Francisella strains (step 1), followed by ATP (step 2), we found no difference in IL-18 release, p20 caspase-1 release and ASC oligomerization between Francisella strains (F. novicida, F. holarctica -LVS and F. tularensis Schu S4). This priming is fast, independent of bacteria viability, internalization and phagosome escape, but requires TLR2-mediated ERK phosphorylation. In contrast to their efficient priming capacity, Francisella strains LVS and Schu S4 were impaired in inflammasome triggering compared to F. novicida. Thus, observed differences in inflammasome activation by F. novicida, LVS and Schu S4 depend not on differences in priming but rather on their propensity to trigger the primed inflammasome.
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