ArticleInfection and immunity2012
The rickettsial OmpB β-peptide of Rickettsia conorii is sufficient to facilitate factor H-mediated serum resistance.
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 17 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
17 citing papers in PubMed, 33 citations in OpenAlex.
- Vaccination-induced neutralizing antibodies in immunocompetent hosts correlate with protection against rickettsiae.NPJ vaccines · 2025Article
- PathogenicJournal of bacteriology · 2024Review
- Identification of an autotransporter peptidase of Rickettsia rickettsii responsible for maturation of surface exposed autotransporters.PLoS pathogens · 2023Article
- Transposon mutagenesis of Rickettsia felis sca1 confers a distinct phenotype during flea infection.PLoS pathogens · 2022Article
- Moonlighting in Rickettsiales: Expanding Virulence Landscape.Tropical medicine and infectious disease · 2022Review
- Article
- Contribution of classical complement activation and IgM to the control of Rickettsia infection.Molecular microbiology · 2021Article
- Mediterranean Spotted Fever: Current Knowledge and Recent Advances.Tropical medicine and infectious disease · 2021Review
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Recent research milestones in the pathogenesis of human rickettsioses and opportunities ahead.Future microbiology · 2020Review
- Evasion of autophagy mediated by Rickettsia surface protein OmpB is critical for virulence.Nature microbiology · 2019Article
- Immunity against the Obligate Intracellular Bacterial Pathogen Rickettsia australis Requires a Functional Complement System.Infection and immunity · 2018Article
- TheFrontiers in cellular and infection microbiology · 2017Article
- Article
- Secretome of obligate intracellular Rickettsia.FEMS microbiology reviews · 2015Review
- Pathogenic Rickettsia species acquire vitronectin from human serum to promote resistance to complement-mediated killing.Cellular microbiology · 2014Article
- Exchange protein directly activated by cAMP plays a critical role in bacterial invasion during fatal rickettsioses.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pathogenic species of the spotted fever group Rickettsia are subjected to repeated exposures to the host complement system through cyclic infections of mammalian and tick hosts. The serum complement machinery is a formidable obstacle for bacteria to overcome if they endeavor to endure this endozoonotic cycle. We have previously demonstrated that that the etiologic agent of Mediterranean spotted fever, Rickettsia conorii, is susceptible to complement-mediated killing only in the presence of specific monoclonal antibodies. We have also shown that in the absence of particular neutralizing antibody, R. conorii is resistant to the effects of serum complement. We therefore hypothesized that the interactions between fluid-phase complement regulators and conserved rickettsial outer membrane-associated proteins are critical to mediate serum resistance. We demonstrate here that R. conorii specifically interacts with the soluble host complement inhibitor, factor H. Depletion of factor H from normal human serum renders R. conorii more susceptible to C3 and membrane attack complex deposition and to complement-mediated killing. We identified the autotransporter protein rickettsial OmpB (rOmpB) as a factor H ligand and further demonstrate that the rOmpB β-peptide is sufficient to mediate resistance to the bactericidal properties of human serum. Taken together, these data reveal an additional function for the highly conserved rickettsial surface cell antigen, rOmpB, and suggest that the ability to evade complement-mediated clearance from the hematogenous circulation is a novel virulence attribute for this class of 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.