ArticleInfection and immunity1998
The (alpha2-->8)-linked polysialic acid capsule and lipooligosaccharide structure both contribute to the ability of serogroup B Neisseria meningitidis to resist the bactericidal activity of normal human serum.
Article in Infection and immunity, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
81 citing papers in PubMed, 157 citations in OpenAlex.
- Efficacy of the serogroup BBMJ open · 2026Article
- Exploring the Scope of FunctionalizedMolecules (Basel, Switzerland) · 2025Article
- Identification of a Kingella kingae factor H binding protein that is the major determinant of serum resistance.PLoS pathogens · 2025Article
- Genetic characterization and estimated 4CMenB vaccine strain coverage of 284Human vaccines & immunotherapeutics · 2024Article
- Article
- Characterization of Unusual Serogroups ofMicroorganisms · 2024Article
- Article
- Low molecular weight polysialic acid binds to properdin and reduces the activity of the alternative complement pathway.Scientific reports · 2022Article
- The Host-Pathogen Interactions and Epicellular Lifestyle ofFrontiers in cellular and infection microbiology · 2022Review
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Molecular insights into meningococcal carriage isolates from Burkina Faso 7 years after introduction of a serogroup A meningococcal conjugate vaccine.Microbial genomics · 2020Article
- Control of Innate Immunity by Sialic Acids in the Nervous Tissue.International journal of molecular sciences · 2020Review
- Atypical, Yet Not Infrequent, Infections withPathogens (Basel, Switzerland) · 2019Review
- Genetics behind the Biosynthesis of Nonulosonic Acid-Containing Lipooligosaccharides in Campylobacter coli.Journal of bacteriology · 2019Article
- Diversity-Generating Machines: Genetics of Bacterial Sugar-Coating.Trends in microbiology · 2018Review
- Characterization of capsule genes in non-pathogenic Neisseria species.Microbial genomics · 2018Article
- Article
- Survival of Neisseria meningitidis outside of the host: environmental effects and differences among strains.Epidemiology and infection · 2017Article
- Emergence of a newProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Molecular characterization of invasive capsule null Neisseria meningitidis in South Africa.BMC microbiology · 2017Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The molecular basis for the resistance of serogroup B Neisseria meningitidis to the bactericidal activity of normal human sera (NHS) was examined with a NHS-resistant, invasive serogroup B meningococcal isolate and genetically and structurally defined capsule-, lipooligosaccharide (LOS)-, and sialylation-altered mutants of the wild-type strain. Expression of the (alpha2-->8)-linked polysialic acid serogroup B capsule was essential for meningococcal resistance to NHS. The very NHS-sensitive phenotype of acapsular mutants (99.9 to 100% killed in 10, 25, and 50% NHS) was not rescued by complete LOS sialylation or changes in LOS structure. However, expression of the capsule was necessary but not sufficient for a fully NHS-resistant phenotype. In an encapsulated background, loss of LOS sialylation by interrupting the alpha2,3 sialyltransferase gene, lst, increased sensitivity to 50% NHS. In contrast, replacement of the lacto-N-neotetraose alpha-chain (Galbeta1-4GlcNAcbeta1-3Galbeta1-4Glc) with glucose extensions (GlcN) in a galE mutant resulted in a strain resistant to killing by 50% NHS at all time points. Encapsulated meningococci expressing a Hep2(GlcNAc)-->KDO2-->lipid A LOS without an alpha-chain demonstrated enhanced sensitivity to 50% NHS (98% killed at 30 min) mediated through the antibody-dependent classical complement pathway. Encapsulated LOS mutants expressing truncated Hep2-->KDO2-->lipid A and KDO2-->lipid A structures were also sensitive to 50% NHS (98 to 100% killed at 30 min) but, unlike the wild-type strain and mutants with larger oligosaccharide structures, they were killed by hypogammaglobulinemic sera. These data indicate that encapsulation is essential but that the LOS structure contributes to the ability of serogroup B N. meningitidis to resist the bactericidal activity of NHS.
Indexed as
Identifiers
What OpenQuestion holds
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.