|
|
|
|||||||
|
|||||||||
(Received for publication, July 5, 1995; and in revised form, February 7, 1996) From the
The type VIII capsular polysaccharide has been isolated and
purified from a newly described strain of group B Streptococcus which is a leading cause of sepsis and neonatal meningitis in
Japan. The polysaccharide contains D-glucose, D-galactose, L-rhamnose, and sialic acid in the molar
ratio 1:1:1:1. By means of high resolution
Enzymatic studies established
this polysaccharide as the first from which sialic acid, linked to a
branched
The group B Streptococcus (GBS) ( The structures of the capsular polysaccharides
of GBS types Ia, Ib, II, III(6) , IV(7) ,
V(8) , VI(9) , and VII (10) have been
elucidated. Despite their structural relatedness they are largely
distinct immunologically. We report the isolation, structural analysis,
and immunochemical characterization of the type VIII GBS capsular
polysaccharide which like all the other type-specific GBS
polysaccharides contains terminal sialic acid.
The absolute configurations
of the monosaccharides were determined by a modification of the method
described by Gerwig et al.(15) . The polysaccharide
sample (1 mg) was hydrolyzed with 0.25 M sulfuric acid at 100
°C for 20 h, and the hydrolyzate was neutralized with barium
carbonate. The sediment was removed by centrifugation and the
supernatant was freeze-dried. The lyophilized residue was dissolved in
0.5 ml of(-)-2-butanol, 1 drop of trifluoroacetic acid was added,
and the mixture was heated at 80 °C for 16 h. The solvents were
removed by evaporation in vacuum and the dried sample was
trimethylsilylated using 0.5 ml of N,O-bis-(trimethylsilyl)acetamide (Pierce) and 0.5 ml of
pyridine. The trimethylsilylated(-)-2-butylglycosides of the
constituent monosaccharides were analyzed by capillary gas-liquid
chromatography using a Varian Saturn II GC-MS instrument equipped with
a DB-17 capillary column (0.25 mm x 30 m, film thickness 0.25 µm)
in the temperature program 150 to 210 °C at 2 °C/min.
Figure 1:
The assignment of the
Figure 2:
Structure of the native (top) and
desialylated (bottom) type VIII polysaccharide antigens of
GBS.
The
sequence of monosaccharides in the repeating unit of both the native
and desialylated type VIII GBS polysaccharides were established from
separate analyses of their two-dimensional-NOESY spectra(18) ,
and the NOE data (Table 1) are consistent with their structures
shown in Fig. 2. Independent confirmation of the sequence of
monosaccharides in the repeating unit of the desialylated
polysaccharide was also obtained using an
Competition ELISA revealed that
rabbit antiserum to whole cells of type VIII strain 130013 had high
affinity for the native type VIII polysaccharide. The concentration of
native type VIII polysaccharide that resulted in a 50% inhibition of
the binding of type VIII-specific antiserum was 2.8 µM (Fig. 3). Desialylated, periodate oxidized/borohydride
reduced, or carbodiimide-reduced type VIII polysaccharide failed to
inhibit binding of type VIII-specific antiserum even when used at a
concentration of 0.5 mM (Fig. 3).
Figure 3:
ELISA
inhibition of GBS type VIII rabbit antiserum with native (closed
circles), carbodiimide-reduced (open circles),
periodate-oxidized/borohydride-reduced (closed squares), and
desialylated (open squares) type VIII polysaccharides. Values
are the mean of duplicate determinations.
The structure of the type VIII polysaccharide represents a
different motif from previously studied capsular polysaccharides of
GBS. Capsular polysaccharides of types Ia, Ib, II, III, IV, V, and VII
are all composed of D-galactose, D-glucose, N-acetyl-D-glucosamine, and N-acetylneuraminic acid and contain complex repeating units
built from five to seven monosaccharides. The type VIII polysaccharide
is not only the first GBS capsular polysaccharide composed of
tetrasaccharide repeating units, but is also unique in that
Although it shares
structural features with other GBS polysaccharides, the type VIII
polysaccharide is antigenically distinct. No significant
cross-reactions were detected by type VIII-specific ELISA after
adsorption of type VIII-specific rabbit antiserum with GBS organisms of
heterologous serotypes. The lack of cross-reactions among the GBS
polysaccharides (7, 8, 28) indicates that
sialic acid is not, in and by itself, an immunodominant epitope. The
failure of sialic acid to be immunodominant might be expected in light
of its ubiquity in human and animal tissues(29) . However, it
is only ``non-immunodominant'' in the classical sense, that
is, not being a direct epitope for antibody binding, but its presence
is still crucial to the immunospecificity of antibody raised to the
native type VIII polysaccharide. This was demonstrated by the inability
of desialylated or otherwise chemically modified type VIII
polysaccharide to bind to a significant extent to type VIII-specific
antibodies. The involvement of sialic acid in the formation of an
immunospecific epitope has also been reported for GBS serotypes Ia, II,
III, and VI(4, 28) , and hypothesized that the
explanation for this specificity lies in the ability of sialic acid to
exert conformational control over the epitopic expression of these
polysaccharides. The epitopic expression based on extended helical
domains of polymers of GBS type II polysaccharide and G All GBS polysaccharides whose structures have been
elucidated possess side chains that are composed of or terminate with
sialic acid. Sialic acid has been shown to be a critical virulence
component (36) of these organisms by limiting the deposition on
cells of C3b for opsonization in the absence of specific
antibodies(37) . That this distinguishing characteristic has
been maintained on all capsular polysaccharides of GBS isolated from
human sources, including type VIII, emphasizes the importance of this
sugar in GBS pathogenesis.
Volume 271,
Number 15,
Issue of April 12, 1996 pp. 8786-8790
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
FOOTNOTES
ACKNOWLEDGEMENTS
REFERENCES
H nuclear
magnetic resonance (H NMR), 
C NMR, and homo-
and heterocorrelated NMR, the repeating unit structure of the type VIII
polysaccharide was delineated as the following,
-D-galactopyranosyl residue, is known to be
removed by bacterial neuraminidase.
)has long
been recognized as a major cause of neonatal sepsis and
meningitis(1, 2) . GBS strains are classified into
serotypes on the basis of their type-specific capsular polysaccharides.
The strains isolated from clinical cases usually belong to one of the
major capsular types (Ia, Ib, II, and III)(2) , but five new
serotypes have recently been described: IV, V(3) ,
VI(4) , VII, and VIII. Type VIII (
)(originally
designated type M9(5) ), while not isolated in North America,
has been identified with increasing frequency over the last six years
among disease-causing isolates in Japan, where it is now a prevalent
strain (5) .
Bacterial Strains and Isolation of the Type VIII
Capsular Polysaccharide
Type VIII GBS strains JM9 Prague No.
130013 and JM9 Prague No. 130672 were kindly provided by Dr. J.
Jelínková, Institute
of Hygiene and Epidemiology, Prague, Czech Republic. Strain 130013 was
used in the production and purification of the type VIII capsular
polysaccharide. GBS strains used in adsorption studies, which had been
maintained at -70 °C in cultures at the Channing Laboratory,
included: 909 (type Ia), H36B (type Ib), 18RS21 (type II), M781 (type
III), M15 (acapsular type III), 3139 (type IV), 1169 (type V), and
SS1214 (type VI). GBS strain 130013 was grown in a 16-liter fermenter
and the type VIII polysaccharide was isolated and purified by methods
utilized previously for other GBS polysaccharides(11) .Analytical Methods
The relative molecular weight
of the purified type VIII polysaccharide was determined by gel
filtration chromatography on a Superose 6 column (Pharmacia) calibrated
with dextran standards. The identity and the immunospecificity of the
polysaccharide were tested in double diffusion (Ouchterlony) assay and
the competition ELISA, respectively, with use of GBS type-specific
antisera. The glycose composition of purified polysaccharide was
assessed by gas-liquid chromatography of component alditol acetates
prepared by acid hydrolysis of capsular polysaccharide, as described
below in the section dealing with the determination of the absolute
configuration of the component monosaccharides. Total carbohydrate
content was determined by the phenol-sulfuric acid assay (12) with galactose used as the standard. Purified capsular
polysaccharides were analyzed for protein by the method of Larson et al. (13) and were studied spectrophotometrically at A
for nucleic acids. The presence and quantity
of sialic acid were determined by the method of Warren (14) after hydrolysis of the purified polysaccharide with 3%
acetic acid (v/v) at 80 °C for 1 h.Preparation of the Chemically Modified Type VIII
Polysaccharide
Desialylated type VIII polysaccharide was
prepared by hydrolysis of the native polysaccharide with 1% acetic acid
at 80 °C for 1 h. After dialysis, the contents of the dialysis bag
were freeze-dried. Carbodiimide reduction and periodate oxidation of
the terminal sialic acid residues in the native type VIII
polysaccharide were conducted as described by Jennings et
al.(16) . If required, the modification procedure was
repeated several times until a completely derivatized product was
obtained, as confirmed by NMR spectroscopy and mass spectrometry.Enzymatic Methods
The relative susceptibilities of
the GBS type II, type III, and type VIII polysaccharides to the action
of neuraminidase (type II from Vibrio cholerae, EC 3.2.1.18,
Sigma) were determined in a following manner: 1 ml of a solution of
each polysaccharide (1 mg/ml) was treated with 5 milliunits of
neuraminidase/mg at 37 °C for 48 h. A 250-µl volume of each
sample was then removed and, after the addition of 16 µl of glacial
acetic acid (final concentration, 6%) was hydrolyzed for 1 h at 80
°C. The amount of sialic acid released by each treatment was
quantified in the thiobarbituric acid assay, as described by Skoza and
Mohos(17) . In other experiments, 1-ml volumes of solutions of
the polysaccharides (1 mg/ml) were treated with 5 or 10 milliunits of
neuraminidase/mg at 37 °C; 200-µl aliquotes were collected
after 8, 24, 32, 48, and 120 h; and the amount of liberated sialic acid
was determined in thiobarbituric acid assay.Instrumental Methods
All NMR experiments were
performed on a Bruker AMX 600 spectrometer using a 5-mm broad band
probe with H coil nearest to the sample. H and C NMR spectra were recorded at 330 K in DO at
pH 7.0. Acetone was used as internal standard, with the CH
resonance at 31.07 ppm for C spectra and 2.225 ppm
for H spectra. The experiments were conducted without
sample spinning. Two-dimensional homo- and heterocorrelated experiments
(COSY, TOCSY, NOESY, HMQC) were carried out as described
previously(18) . HMQC-TOCSY experiment was performed according
to Lerner and Bax (19) and H-detected multiple-bond
correlation experiment was carried out by the method of Bax and Summers (20) . Spin-echo Fourier transformation experiment was
conducted using an interleaved decoupling during the spin-echo
period(21) .Antisera
Type-specific antisera to polysaccharides
of GBS types Ia, Ib, II, and III were obtained by the immunization of
New Zealand White rabbits with GBS polysaccharide-tetanus toxoid
conjugate vaccines(22, 23, 24) .
Formalin-killed GBS cells of serotypes IV, V, VI, and VIII (strain JM9
Prague No. 130013) were used as whole cell immunogens for the
preparation of rabbit antisera by the method of Lancefield et
al.(25) . Rabbit antiserum to Streptococcus pneumonia type 14 was prepared by the Staten Seruminstitut (Copenhagen) and
obtained through Dako Corp. (Santa Barbara, CA).Serotype Specificity of Rabbit Antiserum to Strain
1300013
Whole GBS cells grown in Columbia broth (Difco) were
used to evaluate the specificity of type VIII antisera. Log phase cells
(1.0 ml: approximately 10
colony-forming units/ml) were
added to rabbit antiserum to type VIII strain 130013 (0.1 ml; diluted
1:10). After 60 min of inoculation at 37 °C, serum was clarified by
centrifugation, adjusted to a total volume of 2 ml with 0.9 ml of
phosphate-buffered saline containing 0.01% NaN, and
sterilized by filtration (filter pore diameter, 0.45 µm). Adsorbed
serum (initial dilution, 1:200) was added to a 96-well microtiter plate
each well of which was coated with 100 ng of purified type VIII
capsular polysaccharide linked to poly-L-lysine(2) ;
this preparation was processed in a standard ELISA, with alkaline
phosphatase-conjugated goat anti-rabbit IgG (diluted 1:3,000) as the
secondary antibody. Plates were developed for 60 min after addition of
the substrate, and A
was measured with an ELISA
reader (Biotek, Winooki, VT). Values were expressed as the percentage
of type VIII-specific antibodies adsorbed relative to quantities of
antibody in an unadsorbed antiserum control.Competition ELISA
The relative affinities of type
VIII antiserum for native, desialylated, and chemically modified type
VIII polysaccharides was evaluated in a competition ELISA.
Polysaccharide inhibitors were subjected to serial 2-fold dilution,
mixed with an equal volume (100 µl) of type VIII antiserum (diluted
1:400), and added to type VIII polysaccharide-coated ELISA wells. The
latter antiserum, kindly provided by Dr. Patricia Ferrieri of the
University of Minnesota, was adsorbed to remove GBS C-protein activity.
Alkaline phosphatase-conjugated goat anti-rabbit IgG was used as the
secondary antibody at a dilution of 1:3,000, and the plate was
incubated at 37 °C for 60 min. Results are expressed as follows: %
inhibition = [(A without inhibitor
- A with inhibitor)/A without inhibitor] 
100.
Structural Analysis of GBS Type VIII
Polysaccharide
The type VIII capsular polysaccharide preparation
was characterized for carbohydrate composition, molecular size,
immunological identity, and impurities. Compositional analysis of the
type VIII polysaccharide showed that it contained L-rhamnose, D-glucose, D-galactose, and N-acetylneuraminic acid (sialic acid) in 1:1:1:0.9 molar
ratio. The sialic acid content was 30% (as determined in the
thiobarbituric acid assay) and the M
was 200,000
(as determined by gel filtration chromatography). In a double diffusion
immunoassay, type VIII polysaccharide formed a single line of identity
with rabbit antiserum to whole cells of GBS type VIII strain 130013.
Type VIII antiserum did not cross-react with purified capsular
polysaccharides of types Ia, Ib, and II through VI. The protein content
of the purified polysaccharide was <3% (w/w). Spectrophotometric
analysis of purified type VIII capsular polysaccharide (1 mg/ml) showed
a strong absorbance at 206 nm that is characteristic of carbohydrate;
absorbances at 260 and 280 nm were indicative of low residual levels of
nucleic acid and protein, respectively. That the type VIII GBS
polysaccharide was composed of the tetrasaccharide repeating units was
deduced from its H NMR spectrum (600 MHz, 330 K) (Fig. 1) which contained three anomeric signals at 4.857
(unresolved doublet), 4.825 (J
= 7.3 Hz),
and 4.740 ppm (J = 7.4 Hz) in the ratio
1:1:1, as well as the signals at 2.734 and 1.822 ppm of the equatorial
and axial H-3 of 
-linked N-acetyl-D-neuraminic
acid, respectively, whose integration was consistent with the presence
of one sialic acid residue in the repeating unit. The presence of a
tetrasaccharide repeating unit was also confirmed by analysis of the C NMR spectrum of the polysaccharide (150 MHz, 330 K)
which exhibited only three signals in the anomeric region at 104.49
(1C), 103.41 (1C), and 101.38 ppm (2C), but the last signal was shown
to contain two overlapping signals as they could be resolved by a
spin-echo Fourier transformation experiment. The signal at 101.28 ppm
was assigned to the anomeric carbon of the
-L-rhamnopyranosyl residue, while the other one at 101.40
ppm originates from a quarternary carbon, and was thus assigned to C-2
of sialic acid. In addition, signals at 174.29, 52.63, and 39.37 ppm
were observed that correspond to C-1, C-5, and C-3 of the sialic acid,
as well as those at 175.83 and 22.87 ppm due to its N-acetyl
group.
H NMR
spectrum of the type VIII GBS capsular polysaccharide. The signal at
2.225 ppm is that of the methyl group of internal acetone. The signal
at about 3.81 ppm belongs to the methylene groups of Tris used in the
buffer solution. The HOD signal is at 4.44
ppm.
H and C NMR
signals was performed using homocorrelated two-dimensional COSY, TOCSY,
and NOESY techniques, as well as the heterocorrelated HMQC and
HMQC-TOCSY methods. The hexose components of the native repeating unit
shown in Fig. 2were designated a, b, and c according to the sequence of their anomeric signals in the H NMR spectrum. N-Acetylneuraminic acid was
designated as unit d. The location of the H-2 signal of unit b at 3.31 ppm (doublet of doublets with large diaxial couplings J = 7.3 Hz, J
= 9.6 Hz) unambiguously characterized unit b as
being -D-glucose. A small coupling constant (J
3 Hz) and very low-field resonance for
H-4, together with a large value of J coupling
for H-1c, characterized unit c as
-D-galactose. By elimination, the remaining unit a was assigned to be -L-rhamnose. Because of the
mannopyranosyl configuration of the rhamnose ring, it was impossible to
determine its anomeric configuration on the basis of J value. However, NOESY experiments (Table 1) showed that the
anomeric protons of all the sugar units had cross-peaks with their
respective H-3 and H-5 resonances. This finding indicated that the
rhamnopyranosyl residue had the -anomeric configuration as well.
The complete assignment of the H and C NMR
signals of the native and desialylated type VIII GBS polysaccharide are
presented in Table 2and Table 3, respectively.
H-detected
multiple-bond correlation experiment which showed cross-peaks between
C-1a and H-4c, C-1b and H-4a, as well as
between C-1c and H-4b. These long-range correlations are
in agreement with the substitution pattern established by the NOESY
experiment. Additional evidence for the position of sialylation (O-3)
to galactose was also obtained from the downfield displacements
exhibited by the H-3 (Table 2) and C-3 (Table 3) signals of
galactose on desialylation of the native type VIII polysaccharide.Immunological Properties
Rabbit antiserum to whole
type VIII cells was determined by adsorption experiments to be specific
for GBS type VIII strains. Type VIII strains 130013 and 130672 bound
>90% of type VIII polysaccharide-specific antibodies, whereas
<30% of type VIII polysaccharide-specific antibodies were adsorbed
with strains of other GBS serotypes.
Susceptibility to Neuraminidase
The susceptibility
of sialic acid to removal by neuraminidase or acid treatment varies
among the known GBS type-specific polysaccharides. Unlike the others,
type II polysaccharide is resistant to removal of sialic acid by
neuraminidase. This resistance of the type II polysaccharide to
neuraminidase cleavage has been believed to be a result of the unique
position of sialic acid directly linked to galactose in the backbone.
The sialic acid residue in the proposed type VIII polysaccharide
structure is similarly situated. However, in contrast to the type II
polysaccharide, the rate of release of free sialic acid from the type
VIII and type III polysaccharides was similar over a 120-h period (Table 4). As previously shown, the type II polysaccharide
remained resistant to neuraminidase digestion. The optimal specific
activity of neuraminidase resulting in >80% release was 5
milliunits/mg of type III polysaccharide and 10 milliunits/mg of type
VIII polysaccharide.
-L- rhamnopyranosyl residues replace the
2-acetamido-2-deoxy--D-glucopyranosyl residues found in
all other GBS type-specific polysaccharides except type VI(9) .
The overall structure of the type VIII polysaccharide most closely
resembles that of the type II polysaccharide (26) in that the D-galactopyranosyl residues are situated in the backbone
rather than in the side chains, the latter being the case in all other
types(6, 7, 8, 9, 10) .
Like all the other GBS capsular polysaccharides, the type VIII
polysaccharide has terminal sialic acid residues linked to O-3
of D-galactopyranosyl residues.-(2
8)-polysialic acid has been well
documented(28, 30, 31) . A similar
explanation could apply to the epitopic expression of some of the GBS
polysaccharides; in the case of the type III polysaccharide, the
chain-length dependence (number of repeating units) of the epitope,
which is a requirement for extended helical
epitopes(28, 32) , has been established(33) .
Evidence for a sialic acid-controlled conformational epitope in the
type III polysaccharide was obtained with NMR spectroscopy which
revealed significant displacements in chemical shifts of carbon signals
remote from sialic acid when the latter was removed(16) .
Similar displacements in signals in the spectrum of the type VIII
polysaccharide have been detected and may indicate the presence of
sialic acid-controlled conformational epitope. Both NMR signals of the
anomeric carbon (Table 3) and anomeric proton (Table 2) of
the polysaccharide's backbone -D-glucopyranosyl
residue were significantly displaced (1.0 and 0.17 ppm, respectively)
when terminal sialic acid was removed. However, attachment of sialic
acid directly to the backbone of the type VIII polysaccharide puts it
in closer proximity to the backbone than it is in the type III
polysaccharide(6, 11) . Therefore, for the type VIII
polysaccharide, these displacements may also be attributable to
deshielding of the anomeric carbon and proton of the
-D-glucopyranosyl residue by the carboxylate group of the
terminal sialic acid.
ganglioside (IINeuAcGgOse
Cer) are known
to have in their structures terminal N-acetylneuraminic acid
residues that are linked directly to O-3 of a branched
-D-galactopyranosyl residues that are resistant to
treatment with neuraminidase(26, 34, 35) .
This resistance has been attributed to steric hindrance of the approach
of the enzyme because sialic acid is attached directly to O-3 of the
backbone -D-galactopyranosyl residues that have vicinal
substituents in position O-2 or O-4(26) . Although the type
VIII polysaccharide also exhibits the above structural features, its
terminal sialic acid is readily removed with neuraminidase. Obviously
this effect is dependent on specific structural features surrounding
-D-galactopyranosyl residues of the type VIII
polysaccharide. In this region type VIII polysaccharide differs in
structure from both type II polysaccharide and G ganglioside; the most pronounced difference is that its backbone
-D-galactopyranosyl residue is linked glycosidically to a
unique -L-rhamnopyranosyl residue. It is interesting to
speculate that the enzymatic source for the biosynthesis of the
rhamnose substitution in the type VIII polysaccharide may have been
from the same enzymes used by all GBS to synthesize the common group
B-specific cell wall associated polysaccharide which consists of L-rhamnose, D-galactose, D-glucitol, and N-acetyl-D-glucosamine arranged in a complex
multiantennary structure of four structurally distinct oligosaccharides (27) .
))
We thank Fred Cooper for the gas chromatography-mass
spectroscopy and Jeff Brown for technical assistance.
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  I. C. Sutcliffe, G. W. Black, and D. J. Harrington Bioinformatic insights into the biosynthesis of the Group B carbohydrate in Streptococcus agalactiae Microbiology, May 1, 2008; 154(5): 1354 - 1363. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. M Willis, M. Gilbert, M.-F. Karwaski, M.-C. Blanchard, and W. W Wakarchuk Characterization of the {alpha}-2,8-polysialyltransferase from Neisseria meningitidis with synthetic acceptors, and the development of a self-priming polysialyltransferase fusion enzyme Glycobiology, February 1, 2008; 18(2): 177 - 186. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Aoyagi, E. E. Adderson, C. E. Rubens, J. F. Bohnsack, J. G. Min, M. Matsushita, T. Fujita, Y. Okuwaki, and S. Takahashi L-Ficolin/Mannose-Binding Lectin-Associated Serine Protease Complexes Bind to Group B Streptococci Primarily through N-Acetylneuraminic Acid of Capsular Polysaccharide and Activate the Complement Pathway Infect. Immun., January 1, 2008; 76(1): 179 - 188. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Cieslewicz, D. Chaffin, G. Glusman, D. Kasper, A. Madan, S. Rodrigues, J. Fahey, M. R. Wessels, and C. E. Rubens Structural and Genetic Diversity of Group B Streptococcus Capsular Polysaccharides Infect. Immun., May 1, 2005; 73(5): 3096 - 3103. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Seepersaud, S. B. Hanniffy, P. Mayne, P. Sizer, R. Le Page, and J. M. Wells Characterization of a Novel Leucine-Rich Repeat Protein Antigen from Group B Streptococci That Elicits Protective Immunity Infect. Immun., March 1, 2005; 73(3): 1671 - 1683. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Lindahl, M. Stalhammar-Carlemalm, and T. Areschoug Surface Proteins of Streptococcus agalactiae and Related Proteins in Other Bacterial Pathogens Clin. Microbiol. Rev., January 1, 2005; 18(1): 102 - 127. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Aoyagi, E. E. Adderson, J. G. Min, M. Matsushita, T. Fujita, S. Takahashi, Y. Okuwaki, and J. F. Bohnsack Role of L-Ficolin/Mannose-Binding Lectin-Associated Serine Protease Complexes in the Opsonophagocytosis of Type III Group B Streptococci J. Immunol., January 1, 2005; 174(1): 418 - 425. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. L. Lewis, V. Nizet, and A. Varki Discovery and characterization of sialic acid O-acetylation in group B Streptococcus PNAS, July 27, 2004; 101(30): 11123 - 11128. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J. Reinscheid, C. Stosser, K. Ehlert, R. W. Jack, K. Moller, B. J. Eikmanns, and G. S. Chhatwal Influence of proteins Bsp and FemH on cell shape and peptidoglycan composition in group B streptococcus Microbiology, October 1, 2002; 148(10): 3245 - 3254. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Le Thomas-Bories, F. Fitoussi, P. Mariani-Kurkdjian, J. Raymond, N. Brahimi, P. Bidet, V. Lefranc, and E. Bingen Clonal Relationship between U.S. and French Serotype V Group B Streptococcus Isolates J. Clin. Microbiol., December 1, 2001; 39(12): 4526 - 4528. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Rioux, D. Martin, H.-W. Ackermann, J. Dumont, J. Hamel, and B. R. Brodeur Localization of Surface Immunogenic Protein on Group B Streptococcus Infect. Immun., August 1, 2001; 69(8): 5162 - 5165. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. A. Albanyan and M. S. Edwards Lectin Site Interaction with Capsular Polysaccharide Mediates Nonimmune Phagocytosis of Type III Group B Streptococci Infect. Immun., October 1, 2000; 68(10): 5794 - 5802. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Sellin, C. Olofsson, S. Håkansson, and M. Norgren Genotyping of the Capsule Gene Cluster (cps) in Nontypeable Group B Streptococci Reveals Two Major cps Allelic Variants of Serotypes III and VII J. Clin. Microbiol., September 1, 2000; 38(9): 3420 - 3428. [Abstract] [Full Text]
|
|
|
|
 |
|
 D. O. Chaffin, S. B. Beres, H. H. Yim, and C. E. Rubens The Serotype of Type Ia and III Group B Streptococci Is Determined by the Polymerase Gene within the Polycistronic Capsule Operon J. Bacteriol., August 15, 2000; 182(16): 4466 - 4477. [Abstract] [Full Text]
|
|
|
|
 |
|
 L. Deng, D. L. Kasper, T. P. Krick, and M. R. Wessels Characterization of the Linkage between the Type III Capsular Polysaccharide and the Bacterial Cell Wall of Group B Streptococcus J. Biol. Chem., March 10, 2000; 275(11): 7497 - 7504. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Areschoug, M. Stalhammar-Carlemalm, C. Larsson, and G. Lindahl Group B Streptococcal Surface Proteins as Targets for Protective Antibodies: Identification of Two Novel Proteins in Strains of Serotype V Infect. Immun., December 1, 1999; 67(12): 6350 - 6357. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Butko, A. Nicholson-Weller, and M. R. Wessels Role of Complement Component C1q in the IgG-Independent Opsonophagocytosis of Group B Streptococcus J. Immunol., September 1, 1999; 163(5): 2761 - 2768. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Takahashi, Y. Aoyagi, E. E. Adderson, Y. Okuwaki, and J. F. Bohnsack Capsular Sialic Acid Limits C5a Production on Type III Group B Streptococci Infect. Immun., April 1, 1999; 67(4): 1866 - 1870. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. W. Navarre and O. Schneewind Surface Proteins of Gram-Positive Bacteria and Mechanisms of Their Targeting to the Cell Wall Envelope Microbiol. Mol. Biol. Rev., March 1, 1999; 63(1): 174 - 229. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Bhushan, B. F. Anthony, and C. E. Frasch Estimation of Group B Streptococcus Type III Polysaccharide-Specific Antibody Concentrations in Human Sera Is Antigen Dependent Infect. Immun., December 1, 1998; 66(12): 5848 - 5853. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. McKenney, J. Hubner, E. Muller, Y. Wang, D. A. Goldmann, and G. B. Pier The ica Locus of Staphylococcus epidermidis Encodes Production of the Capsular Polysaccharide/Adhesin Infect. Immun., October 1, 1998; 66(10): 4711 - 4720. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Wang, R. I. Hollingsworth, and D. L. Kasper Ozonolysis for selectively depolymerizing polysaccharides containing beta -D-aldosidic linkages PNAS, June 9, 1998; 95(12): 6584 - 6589. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Cieslewicz, D. L. Kasper, Y. Wang, and M. R. Wessels Functional Analysis in Type Ia Group B Streptococcus of a Cluster of Genes Involved in Extracellular Polysaccharide Production by Diverse Species of Streptococci J. Biol. Chem., January 5, 2001; 276(1): 139 - 146. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |