ArticleFrontiers in microbiology2010
Exploitation of host cell biology and evasion of immunity by francisella tularensis.
Article in Frontiers in microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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
30 citing papers in PubMed, 39 citations in OpenAlex.
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- Risk1, a Phosphatidylinositol 3-Kinase Effector, Promotes Rickettsia typhi Intracellular Survival.mBio · 2020Article
- Cathepsins in Bacteria-Macrophage Interaction: Defenders or Victims of Circumstance?Frontiers in cellular and infection microbiology · 2020Review
- CD200R deletion promotes a neutrophil niche for Francisella tularensis and increases infectious burden and mortality.Nature communications · 2019Article
- Discovery and Characterization of Two Classes of Selective Inhibitors of the Suppressor of the TCR Signaling Family of Proteins.ACS infectious diseases · 2019Article
- How Viral and Intracellular Bacterial Pathogens Reprogram the Metabolism of Host Cells to Allow Their Intracellular Replication.Frontiers in cellular and infection microbiology · 2019Review
- Challenges of Francisella classification exemplified by an atypical clinical isolate.Diagnostic microbiology and infectious disease · 2018Article
- Deletion of the Major Facilitator Superfamily TransporterInfection and immunity · 2018Article
- The Early Dendritic Cell Signaling Induced by VirulentMolecular & cellular proteomics : MCP · 2018Article
- Increased Resistance to Intradermal Francisella tularensis LVS Infection by Inactivation of the Sts Phosphatases.Infection and immunity · 2017Article
- Early Interactions of Murine Macrophages with Francisella tularensis Map to Mouse Chromosome 19.mBio · 2016Article
- Francisella tularensis Catalase Restricts Immune Function by Impairing TRPM2 Channel Activity.The Journal of biological chemistry · 2016Article
- F. novicida-Infected A. castellanii Does Not Enhance Bacterial Virulence in Mice.Frontiers in cellular and infection microbiology · 2016Article
- Using host-pathogen protein interactions to identify and characterize Francisella tularensis virulence factors.BMC genomics · 2015Article
- The Divergent Intracellular Lifestyle of Francisella tularensis in Evolutionarily Distinct Host Cells.PLoS pathogens · 2015Review
- Cholera toxin B induced activation of murine macrophages exposed to a fixed bacterial immunogen.Therapeutic advances in vaccines · 2015Article
- The complex amino acid diet of Francisella in infected macrophages.Frontiers in cellular and infection microbiology · 2015Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Francisella tularensis is an intracellular bacterium that infects humans and many small mammals. During infection, F. tularensis replicates predominantly in macrophages but also proliferate in other cell types. Entry into host cells is mediate by various receptors. Complement-opsonized F. tularensis enters into macrophages by looping phagocytosis. Uptake is mediated in part by Syk, which may activate actin rearrangement in the phagocytic cup resulting in the engulfment of F. tularensis in a lipid raft rich phagosome. Inside the host cells, F. tularensis resides transiently in an acidified late endosome-like compartment before disruption of the phagosomal membrane and escape into the cytosol, where bacterial proliferation occurs. Modulation of phagosome biogenesis and escape into the cytosol is mediated by the Francisella pathogenicity island-encoded type VI-like secretion system. Whilst inside the phagosome, F. tularensis temporarily induce proinflammatory cytokines in PI3K/Akt-dependent manner, which is counteracted by the induction of SHIP that negatively regulates PI3K/Akt activation and promotes bacterial escape into the cytosol. Interestingly, F. tularensis subverts CD4 T cells-mediated killing by inhibiting antigen presentation by activated macrophages through ubiquitin-dependent degradation of MHC II molecules on activated macrophages. In the cytosol, F. tularensis is recognized by the host cell inflammasome, which is down-regulated by F. tularensis that also inhibits caspase-1 and ASC activity. During late stages of intracellular proliferation, caspase-3 is activated but apoptosis is delayed through activation of NF-κB and Ras, which ensures cell viability.
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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.