ArticleJournal of leukocyte biology2010
Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis.
Article in Journal of leukocyte biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 99 citations in OpenAlex.
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- Tularemia - a re-emerging disease with growing concern.The veterinary quarterly · 2023Article
- Microbes and the fate of neutrophils.Immunological reviews · 2023Review
- Host-directed therapy for bacterial infections -Modulation of the phagolysosome pathway.Frontiers in immunology · 2023Review
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- Neutrophil Survival Signaling DuringFrontiers in cellular and infection microbiology · 2022Article
- Offense and Defense in Granulomatous Inflammation Disease.Frontiers in cellular and infection microbiology · 2022Review
- Metabolic Reprogramming Mediates Delayed Apoptosis of Human Neutrophils Infected WithFrontiers in immunology · 2022Article
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- Macrophage Selenoproteins Restrict Intracellular Replication ofFrontiers in immunology · 2021Article
- Production of Neutrophil Extracellular Traps Contributes to the Pathogenesis ofFrontiers in immunology · 2020Article
- Cell intrinsic functions of neutrophils and their manipulation by pathogens.Current opinion in immunology · 2019Review
- CD200R deletion promotes a neutrophil niche for Francisella tularensis and increases infectious burden and mortality.Nature communications · 2019Article
- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Ft is a facultative intracellular pathogen that infects many cell types, including neutrophils. In previous work, we demonstrated that the type B Ft strain LVS disrupts NADPH oxidase activity throughout human neutrophils, but how this is achieved is incompletely defined. Here, we used several type A and type B strains to demonstrate that Ft-mediated NADPH oxidase inhibition is more complex than appreciated previously. We confirm that phagosomes containing Ft opsonized with AS exclude flavocytochrome b(558) and extend previous results to show that soluble phox proteins were also affected, as indicated by diminished phosphorylation of p47(phox) and other PKC substrates. However, a different mechanism accounts for the ability of Ft to inhibit neutrophil activation by formyl peptides, Staphylococcus aureus, OpZ, and phorbol esters. In this case, enzyme targeting and assembly were normal, and impaired superoxide production was characterized by sustained membrane accumulation of dysfunctional NADPH oxidase complexes. A similar post-assembly inhibition mechanism also diminished the ability of anti-Ft IS to confer neutrophil activation and bacterial killing, consistent with the limited role for antibodies in host defense during tularemia. Studies of mutants that we generated in the type A Ft strain Schu S4 demonstrate that the regulatory factor fevR is essential for NADPH oxidase inhibition, whereas iglI and iglJ, candidate secretion system effectors, and the acid phosphatase acpA are not. As Ft uses multiple mechanisms to block neutrophil NADPH oxidase activity, our data strongly suggest that this is a central aspect of virulence.
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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.