ArticleInfection and immunity2011
IglG and IglI of the Francisella pathogenicity island are important virulence determinants of Francisella tularensis LVS.
Article in Infection and immunity, 2011. 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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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Functional characterization ofFrontiers in cellular and infection microbiology · 2024Article
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- Type VI Secretion System and Its Effectors PdpC, PdpD, and OpiA Contribute toInfection and immunity · 2021Article
- Control ofMicroorganisms · 2020Review
- Article
- Guanylate-Binding Proteins Are Critical for Effective Control ofFrontiers in cellular and infection microbiology · 2020Article
- Exploring the Diversity Within the GenusFrontiers in microbiology · 2020Article
- ClpB mutants of Francisella tularensis subspecies holarctica and tularensis are defective for type VI secretion and intracellular replication.Scientific reports · 2018Article
- TheFrontiers in cellular and infection microbiology · 2018Review
- Francisella tularensis type VI secretion system comes of age.Virulence · 2017Article
- Article
- Lack of OxyR and KatG Results in Extreme Susceptibility ofFrontiers in cellular and infection microbiology · 2017Article
- Differential Growth ofFrontiers in microbiology · 2017Article
- Francisella tularensis IglG Belongs to a Novel Family of PAAR-Like T6SS Proteins and Harbors a Unique N-terminal Extension Required for Virulence.PLoS pathogens · 2016Article
- Microinjection of Francisella tularensis and Listeria monocytogenes reveals the importance of bacterial and host factors for successful replication.Infection and immunity · 2015Article
- From the Outside-In: The Francisella tularensis Envelope and Virulence.Frontiers in cellular and infection microbiology · 2015Review
- FipB, an essential virulence factor of Francisella tularensis subsp. tularensis, has dual roles in disulfide bond formation.Journal of bacteriology · 2014Article
- Identification of mechanisms for attenuation of the FSC043 mutant of Francisella tularensis SCHU S4.Infection and immunity · 2014Article
- Bacterial programming of host responses: coordination between type I interferon and cell death.Frontiers in microbiology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Gram-negative bacterium Francisella tularensis is the causative agent of tularemia, a disease intimately associated with the multiplication of the bacterium within host macrophages. This in turn requires the expression of Francisella pathogenicity island (FPI) genes, believed to encode a type VI secretion system. While the exact functions of many of the components have yet to be revealed, some have been found to contribute to the ability of Francisella to cause systemic infection in mice as well as to prevent phagolysosomal fusion and facilitate escape into the host cytosol. Upon reaching this compartment, the bacterium rapidly multiplies, inhibits activation of the inflammasome, and ultimately causes apoptosis of the host cell. In this study, we analyzed the contribution of the FPI-encoded proteins IglG, IglI, and PdpE to the aforementioned processes in F. tularensis LVS. The ΔpdpE mutant behaved similarly to the parental strain in all investigated assays. In contrast, ΔiglG and ΔiglI mutants, although they were efficiently replicating in J774A.1 cells, both exhibited delayed phagosomal escape, conferred a delayed activation of the inflammasome, and exhibited reduced cytopathogenicity as well as marked attenuation in the mouse model. Thus, IglG and IglI play key roles for modulation of the intracellular host response and also for the virulence of F. tularensis.
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