ArticlePloS one2009
TLR-dependent control of Francisella tularensis infection and host inflammatory responses.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 56 citations in OpenAlex.
- Article
- Article
- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
- Article
- Bacterial lipoproteins and other factors released by Francisella tularensis modulate human neutrophil lifespan: Effects of a TLR1 SNP on apoptosis inhibition.Cellular microbiology · 2018Article
- Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein DuringFrontiers in immunology · 2018Article
- Hematopoietic MyD88 and IL-18 are essential for IFN-γ-dependent restriction of type AJournal of leukocyte biology · 2017Article
- Toll-like receptor 2 has a prominent but nonessential role in innate immunity toPhysiological reports · 2017Article
- Article
- Innate Immune Recognition: Implications for the Interaction ofFrontiers in cellular and infection microbiology · 2017Review
- Efficacy of Resistance toFrontiers in immunology · 2017Article
- Toll-Like Receptor 2 Recognizes Orientia tsutsugamushi and Increases Susceptibility to Murine Experimental Scrub Typhus.Infection and immunity · 2016Article
- Mitogen-activated protein kinases (MAPKs) are modulated during Francisella tularensis infection, but inhibition of extracellular-signal-regulated kinases (ERKs) is of limited therapeutic benefit.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016Article
- Microinjection of Francisella tularensis and Listeria monocytogenes reveals the importance of bacterial and host factors for successful replication.Infection and immunity · 2015Article
- Depletion of alveolar macrophages in CD11c diphtheria toxin receptor mice produces an inflammatory response.Immunity, inflammation and disease · 2015Article
- Entry of Francisella tularensis into Murine B Cells: The Role of B Cell Receptors and Complement Receptors.PloS one · 2015Article
- Inflammasome priming is similar for francisella species that differentially induce inflammasome activation.PloS one · 2015Article
- Comparative review of Francisella tularensis and Francisella novicida.Frontiers in cellular and infection microbiology · 2014Review
- TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB.Frontiers in immunology · 2014Article
- Host-pathogen interactions and immune evasion strategies in Francisella tularensis pathogenicity.Infection and drug resistance · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundFrancisella tularensis is the causative agent of tularemia and is classified as a Category A select agent. Recent studies have implicated TLR2 as a critical element in the host protective response to F. tularensis infection, but questions remain about whether TLR2 signaling dominates the response in all circumstances and with all species of Francisella and whether F. tularensis PAMPs are predominantly recognized by TLR2/TLR1 or TLR2/TLR6. To address these questions, we have explored the role of Toll-like receptors (TLRs) in the host response to infections with F. tularensis Live Vaccine Strain (LVS) and F. tularensis subspecies (subsp.) novicida in vivo. METHODOLOGY/PRINCIPAL
findingsC57BL/6 (B6) control mice and TLR- or MyD88-deficient mice were infected intranasally (i.n.) or intradermally (i.d.) with F. tularensis LVS or with F. tularensis subsp. novicida. B6 mice survived >21 days following infection with LVS by both routes and survival of TLR1(-/-), TLR4(-/-), and TLR6(-/-) mice infected i.n. with LVS was equivalent to controls. Survival of TLR2(-/-) and MyD88(-/-) mice, however, was significantly reduced compared to B6 mice, regardless of the route of infection or the subspecies of F. tularensis. TLR2(-/-) and MyD88(-/-) mice also showed increased bacterial burdens in lungs, liver, and spleen compared to controls following i.n. infection. Primary macrophages from MyD88(-/-) and TLR2(-/-) mice were significantly impaired in the ability to secrete TNF and other pro-inflammatory cytokines upon ex vivo infection with LVS. TNF expression was also impaired in vivo as demonstrated by analysis of bronchoalveolar lavage fluid and by in situ immunofluorescent staining. CONCLUSIONS/SIGNIFICANCE: We conclude from these studies that TLR2 and MyD88, but not TLR4, play critical roles in the innate immune response to F. tularensis infection regardless of the route of infection or the subspecies. Moreover, signaling through TLR2 does not depend exclusively on TLR1 or TLR6 during F. tularensis LVS infection.
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