ArticleInfection and immunity2013
Importance of PdpC, IglC, IglI, and IglG for modulation of a host cell death pathway induced by Francisella tularensis.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Host-pathogen interactions involved in erythrocyte invasion byFrontiers in cellular and infection microbiology · 2025Article
- Modern Development and Production of a New Live Attenuated Bacterial Vaccine, SCHU S4Pathogens (Basel, Switzerland) · 2021Article
- Development, Phenotypic Characterization and Genomic Analysis of aFrontiers in microbiology · 2021Article
- Guanylate-Binding Proteins Are Critical for Effective Control ofFrontiers in cellular and infection microbiology · 2020Article
- An Overview of Anti-Eukaryotic T6SS Effectors.Frontiers in cellular and infection microbiology · 2020Review
- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
- Article
- Francisella requires dynamic type VI secretion system and ClpB to deliver effectors for phagosomal escape.Nature communications · 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
- An Immature Myeloid/Myeloid-Suppressor Cell Response Associated with Necrotizing Inflammation Mediates Lethal Pulmonary Tularemia.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
- Macrophage cell death upon intracellular bacterial infection.Macrophage · 2015Article
- 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
- Francisella novicida pathogenicity island encoded proteins were secreted during infection of macrophage-like cells.PloS one · 2014Article
- A method for functional trans-complementation of intracellular Francisella tularensis.PloS one · 2014Article
- IglE is an outer membrane-associated lipoprotein essential for intracellular survival and murine virulence of type A Francisella tularensis.Infection and immunity · 2013Article
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
Modulation of host cell death pathways appears to be a prerequisite for the successful lifestyles of many intracellular pathogens. The facultative intracellular bacterium Francisella tularensis is highly pathogenic, and effective proliferation in the macrophage cytosol leading to host cell death is a requirement for its virulence. To better understand the prerequisites of this cell death, macrophages were infected with the F. tularensis live vaccine strain (LVS), and the effects were compared to those resulting from infections with deletion mutants lacking expression of either of the pdpC, iglC, iglG, or iglI genes, which encode components of the Francisella pathogenicity island (FPI), a type VI secretion system. Within 12 h, a majority of the J774 cells infected with the LVS strain showed production of mitochondrial superoxide and, after 24 h, marked signs of mitochondrial damage, caspase-9 and caspase-3 activation, phosphatidylserine expression, nucleosome formation, and membrane leakage. In contrast, neither of these events occurred after infection with the ΔiglI or ΔiglC mutants, although the former strain replicated. The ΔiglG mutant replicated effectively but induced only marginal cytopathogenic effects after 24 h and intermediate effects after 48 h. In contrast, the ΔpdpC mutant showed no replication but induced marked mitochondrial superoxide production and mitochondrial damage, caspase-3 activation, nucleosome formation, and phosphatidylserine expression, although the effects were delayed compared to those obtained with LVS. The unique phenotypes of the mutants provide insights regarding the roles of individual FPI components for the modulation of the cytopathogenic effects resulting from the F. tularensis infection.
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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.