ArticleJournal of innate immunity2014
Virulent Francisella tularensis destabilize host mRNA to rapidly suppress inflammation.
Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 15 citations in OpenAlex.
- Lactate metabolism is exploited bymBio · 2025Article
- Macrophage fate: to kill or not to kill?Infection and immunity · 2024Review
- Protective potential of outer membrane vesicles derived from a virulent strain ofFrontiers in microbiology · 2024Article
- Article
- A study of innate immune kinetics reveals a role for a chloride transporter in a virulent Francisella tularensis type B strain.MicrobiologyOpen · 2021Article
- Article
- Macrophages Demonstrate Guanylate-Binding Protein-Dependent and Bacterial Strain-Dependent Responses toFrontiers in cellular and infection microbiology · 2021Article
- A predictedVirulence · 2019Article
- Unique Francisella Phosphatidylethanolamine Acts as a Potent Anti-Inflammatory Lipid.Journal of innate immunity · 2018Article
- Primary macrophages and J774 cells respond differently to infection with Mycobacterium tuberculosis.Scientific reports · 2017Article
- Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Highly virulent bacterial pathogens have evolved rapid means to suppress host inflammatory responses by unknown mechanisms. Here, we use virulent Francisella tularensis, the cause of lethal tularemia in humans, as a model to elucidate these mechanisms. We show that following infection of murine macrophages F. tularensis rapidly and selectively destabilizes mRNA containing adenylate-uridylate-rich elements that encode for cytokines and chemokines important in controlling bacterial infection. Degradation of host mRNA encoding interleukin (IL)-1β, IL-6 and CXCL1 did not require viable bacteria or de novo protein synthesis, but did require escape of intracellular organisms from endocytic vesicles into the host cytosol. The specific targeting of host mRNA encoding inflammatory cytokines and chemokines for decay by a bacterial pathogen has not been previously reported. Thus, our findings represent a novel strategy by which a highly virulent pathogen modulates host inflammatory responses critical to the evasion of innate immunity.
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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.