ArticleMicrobial pathogenesis2008
A conserved and immunodominant lipoprotein of Francisella tularensis is proinflammatory but not essential for virulence.
Article in Microbial pathogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Tularemia in New York, USA, 1993-2023.Emerging infectious diseases · 2026Article
- Host-pathogen interactions involved in erythrocyte invasion byFrontiers in cellular and infection microbiology · 2025Article
- Development, Strategies, and Challenges for Tularemia Vaccine.Current microbiology · 2024Review
- Article
- Protection induced by a Francisella tularensis subunit vaccine delivered by glucan particles.PloS one · 2018Article
- Identification of disulfide bond isomerase substrates reveals bacterial virulence factors.Molecular microbiology · 2014Article
- TLR2 Signaling is Required for the Innate, but Not Adaptive Response to LVS clpB.Frontiers in immunology · 2014Article
- Large scale structural rearrangement of a serine hydrolase from Francisella tularensis facilitates catalysis.The Journal of biological chemistry · 2013Article
- Identification of Francisella novicida mutants that fail to induce prostaglandin E(2) synthesis by infected macrophages.Frontiers in microbiology · 2013Article
- Roles of chaperone/usher pathways of Yersinia pestis in a murine model of plague and adhesion to host cells.Infection and immunity · 2012Article
- Subversion of host recognition and defense systems by Francisella spp.Microbiology and molecular biology reviews : MMBR · 2012Review
- A mucosal subunit vaccine protects against lethal respiratory infection with Francisella tularensis LVS.PloS one · 2012Article
- Interferon-γ influences the composition of leukocytic infiltrates in murine lyme carditis.The American journal of pathology · 2011Article
- Article
- GroEL and lipopolysaccharide from Francisella tularensis live vaccine strain synergistically activate human macrophages.Infection and immunity · 2010Article
- A tolC mutant of Francisella tularensis is hypercytotoxic compared to the wild type and elicits increased proinflammatory responses from host cells.Infection and immunity · 2010Article
- The francisella tularensis proteome and its recognition by antibodies.Frontiers in microbiology · 2010Article
- Working toward the future: insights into Francisella tularensis pathogenesis and vaccine development.Microbiology and molecular biology reviews : MMBR · 2009Review
- TLR-dependent control of Francisella tularensis infection and host inflammatory responses.PloS one · 2009Article
- Francisella tularensis infection-derived monoclonal antibodies provide detection, protection, and therapy.Clinical and vaccine immunology : CVI · 2009Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Francisella tularensis is a highly virulent bacterium that causes tularemia, a disease that is often fatal if untreated. A live vaccine strain (LVS) of this bacterium is attenuated for virulence in humans but produces lethal disease in mice. F. tularensis has been classified as a Category A agent of bioterrorism. Despite this categorization, little is known about the components of the organism that are responsible for causing disease in its hosts. Here, we report the deletion of a well-characterized lipoprotein of F. tularensis, designated LpnA (also known as Tul4), in the LVS. An LpnA deletion mutant was comparable to the wild-type strain in its ability to grow intracellularly and cause lethal disease in mice. Additionally, mice inoculated with a sublethal dose of the mutant strain were afforded the same protection against a subsequent lethal challenge with the LVS as were mice initially administered a sublethal dose of the wild-type bacterium. The LpnA-deficient strain showed an equivalent ability to promote secretion of chemokines by human monocyte-derived macrophages as its wild-type counterpart. However, recombinant LpnA potently stimulated primary cultures of human macrophages in a Toll-like receptor 2-dependent manner. Although human endothelial cells were also activated by recombinant LpnA, their response was relatively modest. LpnA is clearly unnecessary for multiple functions of the LVS, but its inflammatory capacity implicates it and other Francisella lipoproteins as potentially important to the pathogenesis of tularemia.
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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.