ArticleThe Journal of biological chemistry2010
Francisella tularensis antioxidants harness reactive oxygen species to restrict macrophage signaling and cytokine production.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 49 citations in OpenAlex.
- Evasion of host antioxidative response via disruption of NRF2 signaling in fatal Ehrlichia-induced liver injury.PLoS pathogens · 2023Article
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- Microbiota mediated plasticity promotes thermal adaptation in the sea anemone Nematostella vectensis.Nature communications · 2022Article
- Immune lymphocytes halt replication of Francisella tularensis LVS within the cytoplasm of infected macrophages.Scientific reports · 2020Article
- Guanylate-Binding Proteins Are Critical for Effective Control ofFrontiers in cellular and infection microbiology · 2020Article
- Contributions of TolC Orthologs toInfection and immunity · 2019Article
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- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
- The Ability to Acquire Iron Is Inversely Related to Virulence and the Protective Efficacy ofFrontiers in microbiology · 2018Article
- Lack of OxyR and KatG Results in Extreme Susceptibility ofFrontiers in cellular and infection microbiology · 2017Article
- FcγR mediates TLR2- and Syk-dependent NLRP3 inflammasome activation by inactivated Francisella tularensis LVS immune complexes.Journal of leukocyte biology · 2016Article
- Elucidation of a mechanism of oxidative stress regulation in Francisella tularensis live vaccine strain.Molecular microbiology · 2016Article
- Article
- Antioxidant Defenses of Francisella tularensis Modulate Macrophage Function and Production of Proinflammatory Cytokines.The Journal of biological chemistry · 2016Article
- Francisella tularensis Catalase Restricts Immune Function by Impairing TRPM2 Channel Activity.The Journal of biological chemistry · 2016Article
- Prior infection with Type A Francisella tularensis antagonizes the pulmonary transcriptional response to an aerosolized Toll-like receptor 4 agonist.BMC genomics · 2015Article
- Hfq plays important roles in virulence and stress adaptation in Cronobacter sakazakii ATCC 29544.Infection and immunity · 2015Article
- Article
- Identification of disulfide bond isomerase substrates reveals bacterial virulence factors.Molecular microbiology · 2014Article
- Involvement of a 1-Cys peroxiredoxin in bacterial virulence.PLoS pathogens · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Francisella tularensis is the etiologic agent of the highly infectious animal and human disease tularemia. Its extreme infectivity and virulence are associated with its ability to evade immune detection, which we now link to its robust reactive oxygen species-scavenging capacity. Infection of primary human monocyte-derived macrophages with virulent F. tularensis SchuS4 prevented proinflammatory cytokine production in the presence or absence of IFN-gamma compared with infection with the attenuated live vaccine strain. SchuS4 infection also blocked signals required for macrophage cytokine production, including Akt phosphorylation, IkappaB alpha degradation, and NF-kappaB nuclear localization and activation. Concomitant with SchuS4-mediated suppression of Akt phosphorylation was an increase in the levels of the Akt antagonist PTEN. Moreover, SchuS4 prevented the H(2)O(2)-dependent oxidative inactivation of PTEN compared with a virulent live vaccine strain. Mutation of catalase (katG) sensitized F. tularensis to H(2)O(2) and enhanced PTEN oxidation, Akt phosphorylation, NF-kappaB activation, and inflammatory cytokine production. Together, these findings suggest a novel role for bacterial antioxidants in restricting macrophage activation through their ability to preserve phosphatases that temper kinase signaling and proinflammatory cytokine production.
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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.