scholarly journals Sialic acid content and surface hydrophobicity of group B streptococci

1993 ◽  
Vol 110 (1) ◽  
pp. 87-94 ◽  
Author(s):  
L. A. Teixeira ◽  
A. M. S. Figueiredo ◽  
B. T. Ferreira ◽  
V. M. L. Alves ◽  
P. E. Nagao ◽  
...  
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Acid Content ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Gas Liquid Chromatography ◽  
Group B Streptococci ◽  
Sialic Acid Content ◽  
Asymptomatic Patients ◽  
Group B

SUMMARYThe sialic acid content and the cell-surface hydrophobicity index of 40 group B streptococci (GBS) strains were assessed. GBS isolated from invasive infections (virulent strains) presented an increased level of sialic acid content (1.4%) when compared with GBS isolated from asymptomatic patients (0.53%). Treatment of GBS strain 85634 with neuraminidase resulted in a decrease (about 25%) in the net negative surface charge as assessed by cell electrophoresis. This finding suggests that sialic acid residues are important anionogenic groups exposed on GBS cell surface.N-acetylneuraminic acid was the only sialic acid derivative characterized in the strain 85634 as evaluated by gas-liquid chromatography. GBS from different serotypes presented a hydrophobic index mean value of 0.9. Even though the sialic acid contributed effectively to the negative charge on GBS cell surface, no difference was observed in the hydrophobic index when virulent and avirulent strains were compared.

scholarly journals Capsular Sialic Acid Limits C5a Production on Type III Group B Streptococci

1999 ◽  
Vol 67 (4) ◽  
pp. 1866-1870 ◽  
Author(s):  
Shinji Takahashi ◽  
Youko Aoyagi ◽  
Elisabeth E. Adderson ◽  
Yoshiyuki Okuwaki ◽  
John F. Bohnsack
Keyword(s):  
Sialic Acid ◽  
Specific Antibody ◽  
Acid Content ◽  
Alternative Pathway ◽  
Group B Streptococcus ◽  
Neonatal Infections ◽  
Group B Streptococci ◽  
Sialic Acid Content ◽  
Type Iii ◽  
Group B

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.

Growth of group B streptococci in human serum leads to increased cell surface sialic acid and decreased activation of the alternative complement pathway

1994 ◽  
Vol 40 (2) ◽  
pp. 99-105 ◽  
Author(s):  
Mark W. Platt ◽  
Norberto Correa Jr. ◽  
Carolyn Mold
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Human Serum ◽  
Group B Streptococcus ◽  
Group B Streptococci ◽  
Sialic Acid Content ◽  
Bacterial Surface ◽  
Type Iii ◽  
Alternative Complement ◽  
Group B

Group B streptococcus type III is a major cause of neonatal death. The terminal sialic acid moiety of the group B streptococcus type specific capsule has been shown to be an important virulence factor. We demonstrate here that bacteria grown in human serum have increased cell surface sialic acid content compared with cells grown in common laboratory media. This sialic acid was removed by incubation with neuraminidase, showing that it was on the bacterial surface. Serum-dependent sialylation was dependent on metabolic activity, as the addition of chloramphenicol reduced the amount of added sialic acid by more than 90%. Probing the cell surface with an antibody specific for group B streptococcus type III capsular sialic acid showed an increase in antibody binding after growth in human serum. This effect could be lowered by incubating serum-grown cells in neuraminidase prior to antibody exposure. A group B streptococcus mutant that when grown in laboratory media lacks cell surface sialic acid showed significant cell surface sialic acid when grown in human serum. This increase was associated with a significantly decreased ability to bind C3 and hence activate the alternative complement pathway.Key words: group B streptococcus, capsule, human serum.

scholarly journals Cell surface hydrophobicity and adherence of a strain of group B streptococci during the post-antibiotic effect of penicillin

2008 ◽  
Vol 50 (4) ◽  
pp. 203-207 ◽  
Author(s):  
Ângela Maria Mendes Araújo ◽  
Ivi Cristina Menezes de Oliveira ◽  
Marcos Corrêa de Mattos ◽  
Leslie C. Benchetrit
Keyword(s):  
Cell Surface ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Bacterial Adherence ◽  
Group B Streptococci ◽  
Bacterial Physiology ◽  
Antibiotic Effect ◽  
Buccal Epithelial Cells ◽  
Group B

The minimum inhibitory concentration and post-antibiotic effects of an antimicrobial agent are parameters to be taken into consideration when determining its dosage schedules. The in vitro post-antibiotic effects on cell surface hydrophobicity and bacterial adherence were examined in one strain of group B streptococci. Exposure of the microorganism for 2 h at 37 °C to 1 x MIC of penicillin induced a PAE of 1.1 h. The cell surface charge of the Streptococcus was altered significantly during the post-antibiotic phase as shown by its ability to bind to xylene: hydrophobicity was decreased. Bacterial adherence to human buccal epithelial cells was also reduced. The results of the present investigation indicate that studies designed to determine therapeutic regimens should evaluate the clinical significance of aspects of bacterial physiology during the post-antibiotic period.

Human X- and Y-bearing sperm differ in cell surface sialic acid content

1984 ◽  
Vol 124 (3) ◽  
pp. 950-955 ◽  
Author(s):  
Satoru Kaneko ◽  
Shigeru Oshio ◽  
Toshifumi Kobayashi ◽  
Rihachi Iizuka ◽  
Hideo Mohri
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Acid Content ◽  
Sialic Acid Content

Role of sialic acid in insulin action and the insulin resistance of diabetes mellitus

1988 ◽  
Vol 255 (2) ◽  
pp. E173-E179 ◽  
Author(s):  
A. I. Salhanick ◽  
J. M. Amatruda
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Sialic Acid ◽  
Cell Surface ◽  
Acid Content ◽  
Insulin Action ◽  
Diabetic Rats ◽  
Hepatic Insulin Resistance ◽  
Sialic Acid Content ◽  
Insulin Responsiveness

Adipocytes treated with neuraminidase show markedly reduced responsiveness to insulin without any alteration in insulin binding. In addition, several studies have separately demonstrated both insulin resistance and decreases in membrane sialic acid content and associated biosynthetic enzymes in diabetes mellitus. In the present study, we investigated the role that sialic acid residues may play in insulin action and in the hepatic insulin resistance associated with nonketotic diabetes. Primary cultures of hepatocytes from normal rats treated with neuraminidase demonstrated a dose-dependent decrease in insulin-stimulated lipogenesis. At a concentration of neuraminidase that decreases insulin action by 50%, 23% of total cellular sialic acid content was released. Neuraminidase-releasable sialic acid was significantly decreased in hepatocytes from diabetic rats and this was associated with significant insulin resistance. Treatment of hepatocytes from diabetic rats with cytidine 5'-monophospho-N-acetylneuraminic acid (CMP-NANA) enhanced insulin responsiveness 39%. The enhanced insulin responsiveness induced by CMP-NANA was blocked by cytidine 5'-monophosphate (CMP) suggesting that the CMP-NANA effect was catalyzed by a cell surface sialyltransferase. CMP reduced neuraminidase-releasable [14C]sialic acid incorporation into hepatocytes by 43%. The data demonstrate a role for cell surface sialic acid residues in hepatic insulin action and support a role for decreased cell surface sialic acid residues in the insulin resistance of diabetes mellitus.

Sign in / Sign up

Export Citation Format

Share Document