ArticleCellular microbiology2014
Pathogenic Rickettsia species acquire vitronectin from human serum to promote resistance to complement-mediated killing.
Article in Cellular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Discerning dangerous gain of function: most gain of function (GoF) research does not involve infectious microbes.Frontiers in bioengineering and biotechnology · 2026Review
- Review
- Recruitment of Vitronectin by Bacterial Pathogens: A Comprehensive Overview.Microorganisms · 2024Review
- Outer membrane protein OMP76 ofVirulence · 2023Article
- Subversion of host cell signaling: The arsenal of Rickettsial species.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Contribution of classical complement activation and IgM to the control of Rickettsia infection.Molecular microbiology · 2021Article
- Review
- The neglected challenge: Vaccination against rickettsiae.PLoS neglected tropical diseases · 2020Review
- Recent research milestones in the pathogenesis of human rickettsioses and opportunities ahead.Future microbiology · 2020Review
- A Pathogen and a Non-pathogen Spotted Fever GroupFrontiers in cellular and infection microbiology · 2019Article
- Immunity against the Obligate Intracellular Bacterial Pathogen Rickettsia australis Requires a Functional Complement System.Infection and immunity · 2018Article
- Article
- Article
- TheFrontiers in cellular and infection microbiology · 2017Article
- Article
- Secretome of obligate intracellular Rickettsia.FEMS microbiology reviews · 2015Review
- RC1339/APRc from Rickettsia conorii is a novel aspartic protease with properties of retropepsin-like enzymes.PLoS pathogens · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Bacteria of the genus Rickettsia are transmitted from arthropod vectors and primarily infect cells of the mammalian endothelial system. Throughout this infectious cycle, the bacteria are exposed to the deleterious effects of serum complement. Using Rickettsia conorii, the etiologic agent of Mediterranean spotted fever (MSF), as a model rickettsial species, we have previously demonstrated that this class of pathogen interacts with human factor H to mediate partial survival in human serum. Herein, we demonstrate that R. conorii also interacts with the terminal complement complex inhibitor vitronectin (Vn). We further demonstrate that an evolutionarily conserved rickettsial antigen, Adr1/RC1281, interacts with human vitronectin and is sufficient to mediate resistance to serum killing when expressed at the outer-membrane of serum sensitive Escherichia coli. Adr1 is an integral outer-membrane protein whose structure is predicted to contain eight membrane-embedded β-strands and four 'loop' regions that are exposed to extracellular milieu. Site-directed mutagenesis of Adr1 revealed that at least two predicted 'loop' regions are required to mediate resistance to complement-mediatedkilling and vitronectin acquisition. These results demonstrate that rickettsial species have evolved multiple mechanisms to evade complement deposition and that evasion of killing in serum is an evolutionarily conserved virulence attribute for this genus of obligate intracellular pathogens.
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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.