ArticleInfection and immunity2010
A tolC mutant of Francisella tularensis is hypercytotoxic compared to the wild type and elicits increased proinflammatory responses from host cells.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 41 citations in OpenAlex.
- Identification and protective efficacy characterization of novel immunogenic antigens for Salmonella Enteritidis vaccines.Poultry science · 2026Article
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- TolC and EmrA1 contribute toJournal of bacteriology · 2024Article
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- Article
- Identification ofFrontiers in cellular and infection microbiology · 2022Article
- A Novel sRNA inFrontiers in cellular and infection microbiology · 2020Article
- Contributions of TolC Orthologs toInfection and immunity · 2019Article
- Characterization of a Unique Outer Membrane Protein Required for Oxidative Stress Resistance and Virulence of Francisella tularensis.Journal of bacteriology · 2018Article
- Bacterial lipoproteins and other factors released by Francisella tularensis modulate human neutrophil lifespan: Effects of a TLR1 SNP on apoptosis inhibition.Cellular microbiology · 2018Article
- Early Interactions of Murine Macrophages with Francisella tularensis Map to Mouse Chromosome 19.mBio · 2016Article
- Temperature-Dependent Gentamicin Resistance of Francisella tularensis is Mediated by Uptake Modulation.Frontiers in microbiology · 2016Article
- Macrophage cell death upon intracellular bacterial infection.Macrophage · 2015Article
- From the Outside-In: The Francisella tularensis Envelope and Virulence.Frontiers in cellular and infection microbiology · 2015Review
- TolC-dependent modulation of host cell death by the Francisella tularensis live vaccine strain.Infection and immunity · 2014Article
- EmrA1 membrane fusion protein of Francisella tularensis LVS is required for resistance to oxidative stress, intramacrophage survival and virulence in mice.Molecular microbiology · 2014Article
- Production of outer membrane vesicles and outer membrane tubes by Francisella novicida.Journal of bacteriology · 2013Article
- Article
- Microbial efflux systems and inhibitors: approaches to drug discovery and the challenge of clinical implementation.The open microbiology journal · 2013Article
- Structure, Function and Regulation of Outer Membrane Proteins Involved in Drug Transport in Enterobactericeae: the OmpF/C - TolC Case.The open microbiology journal · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The highly infectious bacterium Francisella tularensis is a facultative intracellular pathogen and the causative agent of tularemia. TolC, which is an outer membrane protein involved in drug efflux and type I protein secretion, is required for the virulence of the F. tularensis live vaccine strain (LVS) in mice. Here, we show that an LVS DeltatolC mutant colonizes livers, spleens, and lungs of mice infected intradermally or intranasally, but it is present at lower numbers in these organs than in those infected with the parental LVS. For both routes of infection, colonization by the DeltatolC mutant is most severely affected in the lungs, suggesting that TolC function is particularly important in this organ. The DeltatolC mutant is hypercytotoxic to murine and human macrophages compared to the wild-type LVS, and it elicits the increased secretion of proinflammatory chemokines from human macrophages and endothelial cells. Taken together, these data suggest that TolC function is required for F. tularensis to inhibit host cell death and dampen host immune responses. We propose that, in the absence of TolC, F. tularensis induces excessive host cell death, causing the bacterium to lose its intracellular replicative niche. This results in lower bacterial numbers, which then are cleared by the increased innate immune response of the host.
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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.