ArticleInfection and immunity2008
The early phagosomal stage of Francisella tularensis determines optimal phagosomal escape and Francisella pathogenicity island protein expression.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 158 citations in OpenAlex.
- Infectious bacteria as biological warfare agents: mechanisms, epidemiological threats, and defense strategies.Frontiers in bioengineering and biotechnology · 2026Review
- Identification of the Francisella novicida FTN_0096 as a factor involved in intracellular replication and host response.PloS one · 2025Article
- Article
- Primary Murine Macrophages as a Tool for Virulence Factor Discovery in Coxiella burnetii.Microbiology spectrum · 2022Article
- ThioredoxinA1 Controls the Oxidative Stress Response of Francisella tularensis Live Vaccine Strain (LVS).Journal of bacteriology · 2022Article
- Vaccination against Bacterial Infections: Challenges, Progress, and New Approaches with a Focus on Intracellular Bacteria.Vaccines · 2022Review
- Identification ofFrontiers in cellular and infection microbiology · 2022Article
- Article
- Further Insight into the Mechanism of Human PMN Lysis following Phagocytosis of Staphylococcus aureus.Microbiology spectrum · 2021Article
- A study of innate immune kinetics reveals a role for a chloride transporter in a virulent Francisella tularensis type B strain.MicrobiologyOpen · 2021Article
- Mechanisms Affecting the Acquisition, Persistence and Transmission ofMicroorganisms · 2020Review
- "Repair Me if You Can": Membrane Damage, Response, and Control from the Viral Perspective.Cells · 2020Review
- Using proteomics to identify host cell interaction partners for VgrG and IglJ.Scientific reports · 2020Article
- Immune lymphocytes halt replication of Francisella tularensis LVS within the cytoplasm of infected macrophages.Scientific reports · 2020Article
- Article
- Expression of Francisella pathogenicity island protein intracellular growth locus E (IglE) in mammalian cells is involved in intracellular trafficking, possibly through microtubule organizing center.MicrobiologyOpen · 2019Article
- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
- Bacterial infections and cancer.EMBO reports · 2018Review
- A Phosphatidylinositol 3-Kinase Effector Alters Phagosomal Maturation to Promote Intracellular Growth of Francisella.Cell host & microbe · 2018Article
- Microbial co-infection alters macrophage polarization, phagosomal escape, and microbial killing.Innate immunity · 2018Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Francisella tularensis is an intracellular pathogen that can survive and replicate within macrophages. Following phagocytosis and transient interactions with the endocytic pathway, F. tularensis rapidly escapes from its original phagosome into the macrophage cytoplasm, where it eventually replicates. To examine the importance of the nascent phagosome for the Francisella intracellular cycle, we have characterized early trafficking events of the F. tularensis subsp. tularensis strain Schu S4 in a murine bone marrow-derived macrophage model. Here we show that early phagosomes containing Schu S4 transiently interact with early and late endosomes and become acidified before the onset of phagosomal disruption. Inhibition of endosomal acidification with the vacuolar ATPase inhibitor bafilomycin A1 or concanamycin A prior to infection significantly delayed but did not block phagosomal escape and cytosolic replication, indicating that maturation of the early Francisella-containing phagosome (FCP) is important for optimal phagosomal escape and subsequent intracellular growth. Further, Francisella pathogenicity island (FPI) protein expression was induced during early intracellular trafficking events. Although inhibition of endosomal acidification mimicked the early phagosomal escape defects caused by mutation of the FPI-encoded IglCD proteins, it did not inhibit the intracellular induction of FPI proteins, demonstrating that this response is independent of phagosomal pH. Altogether, these results demonstrate that early phagosomal maturation is required for optimal phagosomal escape and that the early FCP provides cues other than intravacuolar pH that determine intracellular induction of FPI proteins.
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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.