ArticleInfection and immunity2011
Phagocytic receptors dictate phagosomal escape and intracellular proliferation of Francisella tularensis.
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 53 papers.
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Who cites it
53 citing papers in PubMed, 85 citations in OpenAlex.
- Activation of B1 B cells by F. tularensis atypical LPS depends on classical complement and C3a.PLoS pathogens · 2025Article
- Identification of theFrontiers in cellular and infection microbiology · 2025Article
- Identification of the Francisella novicida FTN_0096 as a factor involved in intracellular replication and host response.PloS one · 2025Article
- A novel method of Francisella infection of epithelial cells using HeLa cells expressing fc gamma receptor.BMC infectious diseases · 2024Article
- Pathogenicity and virulence ofVirulence · 2023Review
- Tularemia - a re-emerging disease with growing concern.The veterinary quarterly · 2023Article
- Immune Targeting of Mycobacteria through Cell Surface Glycan Engineering.ACS chemical biology · 2023Article
- The O-Ag Antibody Response to Francisella Is Distinct in Rodents and Higher Animals and Can Serve as a Correlate of Protection.Pathogens (Basel, Switzerland) · 2021Article
- Host Immunity andMicroorganisms · 2021Review
- Review
- Why Does SARS-CoV-2 Infection Induce Autoantibody Production?Pathogens (Basel, Switzerland) · 2021Article
- Using proteomics to identify host cell interaction partners for VgrG and IglJ.Scientific reports · 2020Article
- Opsonophagocytosis of Chlamydia pneumoniae by Human Monocytes and Neutrophils.Infection and immunity · 2020Article
- Inhibition of Francisella tularensis phagocytosis using a novel anti-LPS scFv antibody fragment.Scientific reports · 2019Article
- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
- Detrimental Influence of Alveolar Macrophages on Protective Humoral Immunity during Francisella tularensis SchuS4 Pulmonary Infection.Infection and immunity · 2018Article
- Francisella philomiragia: Think of Chronic Granulomatous Disease.Journal of clinical immunology · 2018Review
- Zinc Acquisition Mechanisms Differ between Environmental and Virulent Francisella Species.Journal of bacteriology · 2018Article
- Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein DuringFrontiers in immunology · 2018Article
- Proteogenomics in Aid of Host-Pathogen Interaction Studies: A Bacterial Perspective.Proteomes · 2017Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Francisella tularensis, the causative agent of tularemia, survives and proliferates within macrophages of the infected host as part of its pathogenic strategy, through an intracellular life cycle that includes phagosomal escape and extensive proliferation within the macrophage cytosol. Various in vitro models of Francisella-macrophage interactions have been developed, using either opsonic or nonopsonic phagocytosis, and have generated discrepant results on the timing and extent of Francisella phagosomal escape. Here we have investigated whether either complement or antibody opsonization of the virulent prototypical type A strain Francisella tularensis subsp. tularensis Schu S4 affects its intracellular cycle within primary murine bone marrow-derived macrophages. Opsonization of Schu S4 with either human serum or purified IgG enhanced phagocytosis but restricted phagosomal escape and intracellular proliferation. Opsonization of Schu S4 with either fresh serum or purified antibodies redirected bacteria from the mannose receptor (MR) to the complement receptor CR3, the scavenger receptor A (SRA), and the Fcγ receptor (FcγR), respectively. CR3-mediated uptake delayed maturation of the early Francisella-containing phagosome (FCP) and restricted phagosomal escape, while FcγR-dependent phagocytosis was associated with superoxide production in the early FCP and restricted phagosomal escape and intracellular growth in an NADPH oxidase-dependent manner. Taken together, these results demonstrate that opsonophagocytic receptors alter the intracellular fate of Francisella by delivering bacteria through phagocytic pathways that restrict phagosomal escape and intracellular proliferation.
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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.