ArticleInfection and immunity2012
Role of Francisella lipid A phosphate modification in virulence and long-term protective immune responses.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
The trial behind it
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
21 citing papers in PubMed, 36 citations in OpenAlex.
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- Pathogenicity and virulence ofVirulence · 2023Review
- Type VI Secretion System and Its Effectors PdpC, PdpD, and OpiA Contribute toInfection and immunity · 2021Article
- Lipid A Structural Divergence inmSphere · 2021Article
- Microbial Lipid A Remodeling Controls Cross-Presentation Efficiency and CD8 T Cell Priming by Modulating Dendritic Cell Function.Infection and immunity · 2021Article
- Article
- Outer Membrane Lipid Secretion and the Innate Immune Response to Gram-Negative Bacteria.Infection and immunity · 2020Review
- Lipopolysaccharide Recognition in the Crossroads of TLR4 and Caspase-4/11 Mediated Inflammatory Pathways.Frontiers in immunology · 2020Review
- Caspase-11 Non-canonical Inflammasomes in the Lung.Frontiers in immunology · 2020Review
- Article
- Cathepsin B modulates lysosomal biogenesis and host defense against Francisella novicida infection.The Journal of experimental medicine · 2016Article
- Modification of the 1-Phosphate Group during Biosynthesis of Capnocytophaga canimorsus Lipid A.Infection and immunity · 2016Article
- Polyphosphate kinases modulate Campylobacter jejuni outer membrane constituents and alter its capacity to invade and survive in intestinal epithelial cells in vitro.Emerging microbes & infections · 2015Article
- Kdo2 -lipid A: structural diversity and impact on immunopharmacology.Biological reviews of the Cambridge Philosophical Society · 2015Review
- From the Outside-In: The Francisella tularensis Envelope and Virulence.Frontiers in cellular and infection microbiology · 2015Review
- Characterization of tetratricopeptide repeat-like proteins in Francisella tularensis and identification of a novel locus required for virulence.Infection and immunity · 2014Article
- Metabolic labeling to characterize the overall composition of Francisella lipid A and LPS grown in broth and in human phagocytes.Innate immunity · 2014Article
- Uncovering the components of the Francisella tularensis virulence stealth strategy.Frontiers in cellular and infection microbiology · 2014Review
- Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock.Science (New York, N.Y.) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Lipopolysaccharide (LPS) structural modifications have been shown to specifically affect the pathogenesis of many gram-negative pathogens. In Francisella, modification of the lipid A component of LPS resulted in a molecule with no to low endotoxic activity. The role of the terminal lipid A phosphates in host recognition and pathogenesis was determined using a Francisella novicida mutant that lacked the 4' phosphatase enzyme (LpxF). The lipid A of this strain retained the phosphate moiety at the 4' position and the N-linked fatty acid at the 3' position on the diglucosamine backbone. Studies were undertaken to determine the pathogenesis of this mutant strain via the pulmonary and subcutaneous routes of infection. Mice infected with the lpxF-null F. novicida mutant by either route survived primary infection and subsequently developed protective immunity against a lethal wild-type (WT) F. novicida challenge. To determine the mechanism(s) by which the host controlled primary infection by the lpxF-null mutant, the role of innate immune components, including Toll-like receptor 2 (TLR2), TLR4, caspase-1, MyD88, alpha interferon (IFN-α), and gamma interferon(IFN-γ), was examined using knockout mice. Interestingly, only the IFN-γ knockout mice succumbed to a primary lpxF-null F. novicida mutant infection, highlighting the importance of IFN-γ production. To determine the role of components of the host adaptive immune system that elicit the long-term protective immune response, T- and B-cell deficient RAG1(-/-) mice were examined. All mice survived primary infection; however, RAG1(-/-) mice did not survive WT challenge, highlighting a role for T and B cells in the protective immune response.
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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.