scholarly journals GBS type III oligosaccharides containing a minimal protective epitope can be turned into effective vaccines by multivalent presentation

Author(s):  
F Carboni ◽  
F Angiolini ◽  
M Fabbrini ◽  
B Brogioni ◽  
A Corrado ◽  
...  

Abstract Recent structural studies demonstrated that the epitope recognized by a monoclonal antibody representative of the protective response against the type III Group B Streptococcus polysaccharide was comprised within two of the repeating units that constitute the full-length native structure. Here we took advantage of this discovery to design a novel vaccine based on multivalent presentation of the identified minimal epitope on a carrier protein. We show that highly glycosylated short oligosaccharide conjugates elicit functional immune responses comparable to the full-length native polysaccharide. The obtained results pave the way to the design of well-defined glycoconjugate vaccines based on short synthetic oligosaccharides.

1992 ◽  
Vol 4 (17) ◽  
pp. 269-278 ◽  
Author(s):  
Lawrence C. Paoletti ◽  
Michael R. Wessels ◽  
Francis Michon ◽  
Harold J. Jennings ◽  
Dennis L. Kasper

PEDIATRICS ◽  
1978 ◽  
Vol 62 (4) ◽  
pp. 620-621
Author(s):  
Gerald W. Fischer ◽  
James W. Bass ◽  
George H. Lowell ◽  
Martin H. Crumrine

The article by Bortolussi et al. on pneumococcal septicemia and meningitis in the neonat (Pediatrics 60:352, September 1977) was of great interest to us, since we have been analyzing the effect of antibody directed against Streptococcus pneumoniae on group B Streptococcus type III. We have recently shown (unpublished data) that antibody directed against S. pneumoniae type 14 precipitates the hot hydrochloric acid-extracted polysaccharide antigen of group B Streptococcus type III. Further studies have shown that this antibody is opsonic for group B Streptococcus type III in an in vitro bactericidal assay and protective in a suckling rat model of group B Streptococcus type III sepsis.1


PEDIATRICS ◽  
1977 ◽  
Vol 60 (4) ◽  
pp. 473-476 ◽  
Author(s):  
Margaret R. Hammerschlag ◽  
Carol J. Baker ◽  
Susan Alpert ◽  
Dennis L. Kasper ◽  
Ingrid Rosner ◽  
...  

Cultures from the vagina, pharynx, and anal canal of 100 healthy girls, 2 months through 15 years of age, were examined for the presence of group B streptococci. Of the 100 participants, 20% were colonized at one or more of these three sites. Pharyngeal colonization was detected in 15% of the girls under 11 years of age and in 5% of those over 11 years of age. Colonization at anogenital sites was observed in 19% of participants under 3 years of age, in 25% of those 11 years of age and older, and in only 4% of those between the ages of 3 and 10 years (P < .025). The concentration of serum antibody directed against the polysaccharide capsular antigen isolated from type III, group B Streptococcus appeared, in part, to be related to increasing age.


1988 ◽  
Vol 158 (2) ◽  
pp. 471-474 ◽  
Author(s):  
L. E. R. Patterson ◽  
C. J. Baker ◽  
M. A. Rench ◽  
M. S. Edwards

2003 ◽  
Vol 71 (12) ◽  
pp. 6857-6863 ◽  
Author(s):  
Elisabeth E. Adderson ◽  
Shinji Takahashi ◽  
Yan Wang ◽  
Jianling Armstrong ◽  
Dylan V. Miller ◽  
...  

ABSTRACT Group B Streptococcus agalactiae bacteria (group B streptococci [GBS]) are the most common cause of serious bacterial infection in newborn infants. The majority of serotype III-related cases of neonatal disease are caused by a genetically related subgroup of bacteria, restriction fragment digest pattern (RDP) type III-3, suggesting that these strains possess unique genes contributing to virulence. We used genomic subtractive hybridization to identify regions of genomic DNA unique to virulent RDP type III-3 GBS strains. Within one of these III-3-specific regions is a 1,506-bp open reading frame, spb1 (surface protein of group B streptococcus 1). A mutant type III GBS strain lacking Spb1 was constructed in virulent RDP type III-3 strain 874391, and the interactions of the wild-type and spb1 isogenic mutant with a variety of epithelial cells important to GBS colonization and infection were compared. While adherence of the spb1 isogenic mutant to A549 respiratory, C2Bbe1 colonic, and HeLa cervical epithelial cells was slightly lower than that of the 874391 strain, invasion of the Spb1− mutant was significantly reduced with these cell lines compared to what was seen with 874391. The defect in epithelial invasion was corrected by supplying spb1 in trans. These observations suggest that Spb1 contributes to the pathogenesis of neonatal GBS infection by mediating internalization of virulent serotype III GBS and confirm that understanding of the population structure of bacteria may lead to insights into the pathogenesis of human infections.


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