ArticleInfection and immunity1999
Capsular sialic acid limits C5a production on type III group B streptococci.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Human Milk Oligosaccharides Inhibit Group B Streptococcal Growth by Binding PcsB, an Essential Cell Wall Separation Protein.JACS Au · 2026Article
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- Group B Streptococcal Neonatal Meningitis.Clinical microbiology reviews · 2022Review
- Group BACS infectious diseases · 2021Article
- Bacterial and Host Determinants of Group B Streptococcal Vaginal Colonization and Ascending Infection in Pregnancy.Frontiers in cellular and infection microbiology · 2021Review
- The Double Life of Group B Streptococcus: Asymptomatic Colonizer and Potent Pathogen.Journal of molecular biology · 2019Review
- Dual actions of group BProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Human Cervical Mucus Plugs Exhibit Insufficiencies in Antimicrobial Activity Towards Group B Streptococcus.The Journal of infectious diseases · 2018Article
- Diminished Capsule Exacerbates Virulence, Blood-Brain Barrier Penetration, Intracellular Persistence, and Antibiotic Evasion of Hyperhemolytic Group B Streptococci.The Journal of infectious diseases · 2018Article
- Implication of Soluble Forms of Cell Adhesion Molecules in Infectious Disease and Tumor: Insights from Transgenic Animal Models.International journal of molecular sciences · 2018Review
- Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches.Frontiers in pediatrics · 2018Review
- Review
- Discovery and characterization of de novo sialic acid biosynthesis in the phylum Fusobacterium.Glycobiology · 2016Article
- Evolutionary inactivation of a sialidase in group B Streptococcus.Scientific reports · 2016Article
- Antibody response specific to the capsular polysaccharide is impaired in Streptococcus suis serotype 2-infected animals.Infection and immunity · 2015Article
- The interplay between Siglecs and sialylated pathogens.Glycobiology · 2014Review
- Group B Streptococcus engages an inhibitory Siglec through sialic acid mimicry to blunt innate immune and inflammatory responses in vivo.PLoS pathogens · 2014Article
- Sialic acids siglec interaction: a unique strategy to circumvent innate immune response by pathogens.The Indian journal of medical research · 2013Review
- Group B Streptococcus and Streptococcus suis capsular polysaccharides induce chemokine production by dendritic cells via Toll-like receptor 2- and MyD88-dependent and -independent pathways.Infection and immunity · 2013Article
- L-ficolin and capsular polysaccharide-specific IgG in cord serum contribute synergistically to opsonophagocytic killing of serotype III and V group B streptococci.Infection and immunity · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The majority of type III group B streptococcus (GBS) human neonatal infections are caused by a genetically related subgroup called III-3. We have proposed that a bacterial enzyme, C5a-ase, contributes to the pathogenesis of neonatal infections with GBS by rapidly inactivating C5a, a potent pro-inflammatory molecule, but many III-3 strains do not express C5a-ase. The amount of C5a produced in serum following incubation with representative type III strains was quantitated in order to better understand the relationship between C5a production and C5a-ase expression. C5a production following incubation of bacteria with serum depleted of antibody to the bacterial surface was inversely proportional to the sialic acid content of the bacterial capsule, with the more heavily sialylated III-3 strains generating less C5a than the less-virulent, less-sialylated III-2 strains. The amount of C5a produced correlated significantly with C3 deposition on each bacterial strain. Repletion with type-specific antibody caused increased C3b deposition and C5a production through alternative pathway activation, but C5a was functionally inactivated by strains that expressed C5a-ase. The increased virulence of III-3 strains compared to that of III-2 strains results at least partially from the higher sialic acid content of III-3 strains, which inhibits both opsonophagocytic killing and C5a production in the absence of type-specific antibody. We propose that C5a-ase is not necessary for III-3 strains to cause invasive disease because the high sialic acid content of III-3 strains inhibits C5a production.
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