ArticleInfection and immunity2003
An attenuated strain of the facultative intracellular bacterium Francisella tularensis can escape the phagosome of monocytic cells.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers.
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Who cites it
186 citing papers in PubMed, 291 citations in OpenAlex.
- Modulatory Role of ATG5 Protein in Immune Modulation During Experimental Tularemia.Microorganisms · 2026Article
- De Novo Design of High-Affinity Miniprotein Binders Targeting Francisella Tularensis Virulence Factor.Angewandte Chemie (International ed. in English) · 2025Article
- Outer membrane tube formation bymBio · 2025Article
- Identification of the Francisella novicida FTN_0096 as a factor involved in intracellular replication and host response.PloS one · 2025Article
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- PdpC, a secreted effector protein of the type six secretion system, is required for erythrocyte invasion byFrontiers in cellular and infection microbiology · 2022Article
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- Disruption of the Francisella noatunensis subsp.Infection and immunity · 2021Article
- More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.Microbiology and molecular biology reviews : MMBR · 2021Review
- A study of innate immune kinetics reveals a role for a chloride transporter in a virulent Francisella tularensis type B strain.MicrobiologyOpen · 2021Article
- Control ofMicroorganisms · 2020Review
- Atg5-Deficient Mice Infected withMicroorganisms · 2020Article
- Modulation of Host Lipid Pathways by Pathogenic Intracellular Bacteria.Pathogens (Basel, Switzerland) · 2020Review
- Immune lymphocytes halt replication of Francisella tularensis LVS within the cytoplasm of infected macrophages.Scientific reports · 2020Article
- OpiA, a Type Six Secretion System Substrate, Localizes to the Cell Pole and Plays a Role in Bacterial Growth and Viability inJournal of bacteriology · 2020Article
- Stochastic dynamics of Francisella tularensis infection and replication.PLoS computational biology · 2020Article
- Fosmidomycin, an inhibitor of isoprenoid synthesis, induces persistence in Chlamydia by inhibiting peptidoglycan assembly.PLoS pathogens · 2019Article
- 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
126 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The facultative intracellular bacterium Francisella tularensis is a highly virulent and contagious organism, and little is known about its intracellular survival mechanisms. We studied the intracellular localization of the attenuated human vaccine strain, F. tularensis LVS, in adherent mouse peritoneal cells, in mouse macrophage-like cell line J774A.1, and in human macrophage cell line THP-1. Confocal microscopy of infected J774A.1 cells indicated that during the first hour of infection the bacteria colocalized with the late endosomal-lysosomal glycoprotein LAMP-1, but within 3 h this colocalization decreased significantly from approximately 60% to 30%. Transmission electron microscopy revealed that >90% of bacteria were not enclosed by a phagosomal membrane after 2 h of infection, and some bacteria were in vacuoles that were only partially surrounded by a limiting membrane. Similar findings were obtained with all three host cell types. Immunoelectron microscopy performed with an F. tularensis LVS-specific polyclonal rabbit antiserum showed that the antiserum stained a thick, evenly distributed capsule-like material in bacteria grown in broth. In contrast, intracellular F. tularensis LVS cells were only marginally stained with this antiserum. Instead, most of the immunoreactive material was diffusely localized in the phagosomes or was associated with the phagosomal membrane. Our findings indicate that F. tularensis LVS is able to escape from the phagosomes of macrophages via a mechanism that may involve degradation of the phagosomal membrane.
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