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PubMed1990

Outer membrane polysaccharide deficiency in two nongliding mutants of Cytophaga johnsonae.

Phenol-extractable polysaccharides firmly associated with the outer membrane of the gliding bacterium Cytophaga johnsonae could be resolved by gel filtration in sodium dodecyl sulfate (SDS) or by SDS-polyacrylamide gel electrophoresis into a high-molecular-weight (H) fraction (excluded by Sephadex G-200) and a low-molecular-weight (L) fraction. Fraction L was rich in components typical of lipid A and the core region of lipopolysaccharide (P, 3-hydroxy fatty acids, and 2-keto-3-deoxyoctonate) and evidently was a lipopolysaccharide with a limited number of distal, repeating polysaccharide units, as judged by SDS-polyacrylamide gel electrophoresis. In relation to total carbohydrate, the H fraction was rich in amino sugar but poor in (possibly devoid of) the lipid A and core components. Two nongliding mutants were highly deficient in the H fraction; one of these was deficient in sulfonolipid but could be cured by provision of a specific sulfonolipid precursor, a process that also resulted in the return of both the H fraction and gliding, as well as the ability to move polystyrene latex spheres over the cell surface. Hence, the polysaccharide may be the component that is directly involved in motility, and the presence of sulfonolipids in the outer membrane is necessary for the synthesis or accumulation of the polysaccharide. This conclusion was reinforced by the fact that the second nongliding, polysaccharide-deficient mutant had a normal sulfonolipid content.

Cell Fractionation↗
PubMed1992

New structural features of the antigenic extracellular polysaccharides of Penicillium and Aspergillus species revealed with exo-beta-D-galactofuranosidase.

To study the structures of the epitopes of the extracellular polysaccharides from Penicillium and Aspergillus species, an exo-beta-D-galactofuranosidase was purified from a commercial crude enzyme preparation from Trichoderma harzianum. Analysis of ring size and linkage position of the galactose residues of the extracellular polysaccharide of Penicillium digitatum, before and after enzymatic treatment, was determined by the reductive-cleavage technique. In addition to terminal and beta (1-5)-linked galactofuranosides, beta (1-6)-linked and beta (1,5,6)-linked branched galactofuranose residues could be identified. After degradation with the purified exo-beta-D-galactofuranosidase, all initial linkages of the galactofuranose residues were still present, but the amount of beta (1-5)-linked galactofuranose residues had decreased considerably. Treatment of the extracellular polysaccharides of Penicillium and Aspergillus species with the purified exo-beta-D-galactofuranosidase resulted in complete disappearance of the enzyme-linked immunosorbent assay reactivity of these polysaccharides, using immunoglobulin G antibodies raised against P. digitatum. Therefore, with the use of this enzyme, it was proved that the beta (1-5)-linked galactofuranosyl residues only are responsible for the antigenicity of the extracellular polysaccharides of Penicillium and Aspergillus molds. A new structural model for the antigenic galactofuranose side chains of the galactomannan from P. digitatum is proposed.

Aspergillus↗
PubMed1992

Purification and determination of the structure of capsular polysaccharide of Vibrio vulnificus M06-24.

Virulence of Vibrio vulnificus has been strongly associated with encapsulation and an opaque colony morphology. Capsular polysaccharide was purified from a whole-cell, phosphate-buffered saline-extracted preparation of the opaque, virulent phase of V. vulnificus M06-24 (M06-24/O) by dialysis, centrifugation, enzymatic digestion, and phenol-chloroform extraction. Nuclear magnetic resonance spectroscopic analysis of the purified polysaccharide showed that the polymer was composed of a repeating structure with four sugar residues per repeating subunit: three residues of 2-acetamido-2,6-dideoxyhexopyranose in the alpha-gluco configuration (QuiNAc) and an additional residue of 2-acetamido hexouronate in the alpha-galactopyranose configuration (GalNAcA). The complete carbohydrate structure of the polysaccharide was determined by heteronuclear nuclear magnetic resonance spectroscopy and by high-performance anion-exchange chromatography. The 1H and 13C nuclear magnetic resonance spectra were completely assigned, and vicinal coupling relationships were used to establish the stereochemistry of each sugar residue, its anomeric configuration, and the positions of the glycosidic linkages. The complete structure is: [----3) QuipNAc alpha-(1----3)-GalpNAcA alpha-(1----3)-QuipNAc alpha-(1----]n QuipNAc alpha-(1----4)-increases The polysaccharide was produced by a translucent phase variant of M06-24 (M06-24/T) but not by a translucent, acapsular transposon mutant (CVD752). Antibodies to the polysaccharide were demonstrable in serum from rabbits inoculated with M06-24/O.

Antigens, Bacterial↗
PubMed1995

Characterization and localization of the KpsE protein of Escherichia coli K5, which is involved in polysaccharide export.

In Escherichia coli with group II capsules, the synthesis and cellular expression of capsular polysaccharide are encoded by the kps gene cluster. This gene cluster is composed of three regions. The central region 2 encodes proteins involved in polysaccharide synthesis, and the flanking regions 1 and 3 direct the translocation of the finished polysaccharide across the cytoplasmic membrane and its surface expression. The kps genes of the K5 polysaccharide, which is a group II capsular polysaccharide, have been cloned and sequenced. Region 1 contains the kpsE, -D, -U, -C, and -S genes. In this communication we describe the KpsE protein, the product of the kpsE gene. A truncated kpsE gene was fused with a truncated beta-galactosidase gene to generate a fusion protein containing the first 375 amino acids of beta-galactosidase and amino acids 67 to 382 of KpsE (KpsE'). This fusion protein was isolated and cleaved with factor Xa, and the purified KpsE' was used to immunize rabbits. Intact KpsE was extracted from the membranes of a KpsE-overexpressing recombinant strain with octyl-beta-glucoside. It was purified by affinity chromatography with immobilized anti-KpsE antibodies. Cytofluorometric analysis using the anti-KpsE antibodies with whole cells and spheroplasts, as well as sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting (immunoblotting) of proteins from spheroplasts and membranes before and after treatment with proteinase K, indicated that the KpsE protein is associated with the cytoplasmic membrane and has an exposed periplasmic domain. By TnphoA mutagenesis and by constructing beta-lactamase fusions to the KpseE protein, it was possible to determine the topology of the KpsE protein within the cytoplasmic membrane.

Amino Acid Sequence↗
PubMed1967

Serological activity of staphylococcal polysaccharide.

The polysaccharide from cell walls of coagulase-positive staphylococci coated both latex particles and tanned red cells for agglutination by human sera and by specific staphylococcal antisera. Treatment with trypsin or autoclaving destroyed the capacity of polysaccharide to coat particles but did not affect precipitation of antibody. Periodic acid destroyed both properties. The teichoic acid portion of the staphylococcal polysaccharide displayed precipitin activity similar to polysaccharide, but it did not coat either latex particles or tanned red cells. Teichoic acid did, however, inhibit specific agglutination of polysaccharide-coated particles or cells.

Acids↗
PubMed1967

Derepression of phosphomannose isomerase by regulator gene mutations involved in capsular polysaccharide synthesis in Escherichia coli K-12.

A regulator gene mutation (capR) that causes increased synthesis of capsular polysaccharide and derepressed synthesis of several enzymes involved in polysaccharide synthesis also derepresses phosphomannose isomerase (PMI) synthesis. In contrast, a second mutation (capS, which maps separately from capR) that causes increased production of the same polysaccharide does not lead to increased synthesis of PMI (nor of several of the other enzymes involved in polysaccharide synthesis). Introduction of the capR9 allele by transduction or mutation of capR(+) to capR can change the phenotype of a mannose-negative nonmucoid strain to a mannose-positive mucoid phenotype. Thus, genotype capR(+)man-2 is mannose-negative and nonmucoid, but genotype capR9 man-2 is mannose positive and mucoid. Other interactions between these alleles in the synthesis of capsular polysaccharide are recorded.

Chromosome Mapping↗
PubMed1992

Seroprevalence of immunoglobulin M (IgM) and IgG antibodies to polysaccharides of Streptococcus pneumoniae in different age groups of Ecuadorian and German children.

The age-specific prevalence of serum immunoglobulin M (IgM) antibody to capsular polysaccharides of Streptococcus pneumoniae, as detected by enzyme-linked immunosorbent assay, was studied in 1,301 Ecuadorian children enrolled in a national nutrition and health survey. This prevalence was 6% in infants < 6 months old and increased to 28% in children 6 to 11 months old, 49% in those 12 to 17 months old, and 58% in those 18 to 23 months old. About 80% of the 5-year-old children had this antibody. When tested separately against six different capsular polysaccharides, serum IgM antibody reacted with decreasing frequency with serotype 3, 8, 19, 6, 23, and 1 capsular polysaccharides. We did not observe a broadening of the antibody response with increasing age in the sense that more and more serotypes were recognized. A similar age-related prevalence was found for IgM antibody to the species-specific C-polysaccharide of S. pneumoniae and for IgG antibody to capsular polysaccharides of S. pneumoniae. A smaller German serum collection showed a comparable age-related prevalence of pneumococcus-specific serum IgG and IgM antibodies. The highest incidence of respiratory diseases was observed in 1- and 2-year-old Ecuadorian children. It thus seems that acquisition of serum antibody to S. pneumoniae reflects more the developmental maturation of an immune response than an actual exposure to different pneumococcal serotypes.

Age Factors↗
PubMed1993

Bacteroides fragilis strains express multiple capsular polysaccharides.

Previous studies by our group have demonstrated that the capsule of Bacteroides fragilis type strain NCTC 9343 consists of two chemically distinct polysaccharides, designated PS A and PS B. These polysaccharides can be isolated as an aggregate from the surface of the organism and give a complex multiprecipitin profile when they are reacted with homologous antiserum in an immunoelectrophoresis assay. Following structural analysis of PS A and PS B, we have determined that the complex precipitin profile is formed as a result of the differing electrophoretic and antigenic properties associated with each of these polymers. Presently, we have examined the capsular polysaccharides of 13 other strains of B. fragilis according to methods used for the prototype strain. The capsules of these strains were extracted, partially purified, and analyzed by immunoelectrophoresis at pH 7.3. Following reaction with homologous polyclonal antisera, each of the capsular preparations tested yielded a complex precipitin profile similar to that of the prototype strain. When reacted by immunoelectrophoresis with polyclonal antiserum to 9343 or with monoclonal antibodies to PS A and PS B, these capsular preparations appeared to be antigenically diverse; some preparations (50%) showed complete or partial cross-reaction. These results suggest that the dual polysaccharide motif seen with the prototype strain is a common feature of B. fragilis strains. In addition, the antigenic heterogeneity of B. fragilis capsular polysaccharides could be used for the development of a serological typing scheme.

Antibodies, Bacterial↗
PubMed1971

Interaction of Pseudomonas bacteriophage 2 with the slime polysaccharide and lipopolysaccharide of Pseudomonas aeruginosa strain B1.

Purified slime polysaccharide B and lipopolysaccharide of Pseudomonas aeruginosa strain BI were shown to possess receptor-like properties in inactivating Pseudomonas phage 2, whereas lipoprotein and glycopeptide fractions were devoid of activity. On a weight basis, slime polysaccharide B was more effective than lipopolysaccharide in inactivating phage. The specificity of the reaction with slime polysaccharide B was indicated by the fact that slime polysaccharide A of P. aeruginosa strain EI failed to inactivate phage 2. Electron micrographs showed phage 2 in typical, tail-first position of attachment on intact cells of strain BI, slime polysaccharide B, and lipopolysaccharide. Tail fibers were discernible during phage attachment.

Adsorption↗
PubMed2001

Aspergillus enzymes involved in degradation of plant cell wall polysaccharides.

Degradation of plant cell wall polysaccharides is of major importance in the food and feed, beverage, textile, and paper and pulp industries, as well as in several other industrial production processes. Enzymatic degradation of these polymers has received attention for many years and is becoming a more and more attractive alternative to chemical and mechanical processes. Over the past 15 years, much progress has been made in elucidating the structural characteristics of these polysaccharides and in characterizing the enzymes involved in their degradation and the genes of biotechnologically relevant microorganisms encoding these enzymes. The members of the fungal genus Aspergillus are commonly used for the production of polysaccharide-degrading enzymes. This genus produces a wide spectrum of cell wall-degrading enzymes, allowing not only complete degradation of the polysaccharides but also tailored modifications by using specific enzymes purified from these fungi. This review summarizes our current knowledge of the cell wall polysaccharide-degrading enzymes from aspergilli and the genes by which they are encoded.

Aspergillus↗
PubMed1995

Detection of C-polysaccharide in serum of patients with Streptococcus pneumoniae bacteraemia.

AIM: To investigate the fate of Streptococcus pneumoniae C-polysaccharide antigen in serum in patients with S pneumoniae bacteraemia. METHOD: In vitro dissociation experiments were performed to demonstrate that C-polysaccharide was masked by ligands in normal and acute phase serum. Serum samples from 22 patients with S pneumoniae bacteraemia were treated to dissociate immune complexes and then tested for C-polysaccharide by enzyme linked immunosorbent assay (ELISA). RESULTS: C-polysaccharide antigen was masked in normal and acute phase serum but could be released by EDTA treatment and detected by ELISA. Antigen was found in six patients ranging in concentration from 2.5 to 200 ng/ml. Patients with detectable antigen were more likely to die than those in whom antigen was not detected. CONCLUSION: This study demonstrates that C-polysaccharide antigen commonly circulates in patients with S pneumoniae bacteraemia but its presence is masked by ligands present in serum.

Acute Disease↗
PubMed1985

Structural studies of the cell wall polysaccharide of Nocardia asteroides R 399.

As with other bacteria belonging to the corynebacteria, mycobacteria, and nocardia group, Nocardia possess in their cell walls a neutral polysaccharide. Structural analysis of the cell wall polysaccharide of Nocardia asteroides R 399 was undertaken. The carbohydrate polymer contained D-arabinose and D-galactose as in mycobacteria. Besides these two carbohydrates we pointed out the occurrence of two additional components: D-glucose and a polyol. This polyol, because of its small amount and its uneasy detection, had been for a long time ignored. It has been proven to be the 6-deoxy-D-altritol or 1-deoxy-D-talitol. The polymer consists of a main strand composed of----5 Araf 1----and----4Galp1----or----5Galf1----; oligoarabinosyl side chains were localized on C3 of an arabinosyl residue. Other shorter ramifications also occur on some galactosyl units. A characterization of the linkage between polysaccharide and peptidoglycan inside the cell wall has also been carried out. The two polymers are joined by a phosphodiester bond which involves 6-deoxyaltritol. As some corynebacteria previously analyzed were also shown to contain mannose (and sometimes glucose), we can conclude that the main skeleton of cell wall polysaccharides of the corynebacteria, mycobacteria, and nocardia group of bacteria is an arabinogalactan; however, individual structural features of the polysaccharide are varying according to the bacterial species. These results might be connected with variations that were observed in immunological analysis.

Arabinose↗
PubMed1988

Bacterial extracellular polysaccharides.

The synthesis of extracellular polysaccharides has been recognized in certain bacterial cultures since the 1880s. It is now apparent that a wide range of bacteria produce these polymers and an equally wide range of chemical structures are possible. Their surface location, together with the range of available monosaccharide combinations, noncarbohydrate substituents, and linkage types, make extracellular polysaccharides excellent agents of diversity. As a result, much effort has been directed towards elucidating their structure in pathogenic bacteria and in enteric organisms in particular. Commercial applications of microbial polysaccharides have now broadened the scope of structural information. Most recently, technological advances in molecular biology have created the possibility of manipulating desired polymer characteristics, and with these advances, our knowledge of the mechanisms of synthesis and regulation of cell surface polysaccharides has improved. Ultimately more information regarding the function of extracellular polysaccharides in natural environments may result.

Bacteria↗
PubMed1985

The structure of the specific capsular polysaccharide of Streptococcus pneumoniae type 11F (American type 11).

The specific polysaccharide of Streptococcus pneumoniae type 11F (American type 11) is composed of 2-acetamido-2-deoxy-D-glucose (one part), D-glucose (one part), D-galactose (two parts), ribitol (one part), phosphate (one part), and O-acetyl (two parts). Hydrolysis, dephosphorylation, periodate oxidation, methylation, optical rotation, and 1H and 13C nuclear magnetic resonance studies showed that the polysaccharide is an unbranched linear polymer of a ribitol-phosphate substituted repeating tetrasaccharide unit having the structure: (Formula: see text). The specific capsular polysaccharides of S. pneumoniae type 11B and 11C (American types 76 and 53) were found to have the same tetrasaccharide repeating unit as the 11F polysaccharide, but differed from it in their mode of O-acetylation and the replacement of the ribitol phosphate by glycerol phosphate in the 11C specific polysaccharide.

Animals↗
PubMed1996

The biochemistry and genetics of capsular polysaccharide production in bacteria.

Bacterial polysaccharides are usually associated with the outer surface of the bacterium. They can form an amorphous layer of extracellular polysaccharide (EPS) surrounding the cell that may be further organized into a distinct structure termed a capsule. Additional polysaccharide molecules such as lipopolysaccharide (LPS) or lipooligosaccharide (LOS) may also decorate the cell surface. Polysaccharide capsules may mediate a number of biological processes, including invasive infections of human beings. Discussed here are the genetics and biochemistry of selected bacterial capsular polysaccharides and the basis of capsule diversity but not the genetics and biochemistry of LPS biosynthesis (for reviews see 100, 140).

Antigens, Bacterial↗
PubMedDate not supplied

Sulfated polysaccharides modulate effects of acidic and basic fibroblast growth factors on repair of injured confluent human vascular endothelium.

Semi-automatic analysis of the repair process of a circular mechanical lesion of confluent human vascular endothelial cells in vitro was used to evaluate the contributions of cell migration and cell proliferation. Standard heparin added to culture medium that contained 30% human serum induced an inhibition of cell migration at the lesion margin during the first day after injury. Several sulfated polysaccharides were tested in the presence of 5% human serum. Standard heparin, low molecular weight heparin, or pentosan polysulfate markedly reduced the rate of lesion regeneration. Cell proliferation, measured by 3H-thymidine incorporation at the lesion margin, and cell migration were both decreased. In contrast, the combination of acidic fibroblast growth factor with a sulfated polysaccharide accelerated the repair process. Basic fibroblast growth factor combined with a sulfated polysaccharide gave a regeneration rate similar to that of the control; however, at 4 days after injury, the residual lesion was the same when basic fibroblast growth factor was used alone or when it was combined with sulfated polysaccharides. Acidic fibroblast growth factor totally reversed the effects of sulfated polysaccharides on the repair process by enhancing endothelial cell proliferation and allowing endothelial cell migration.

Autoradiography↗
PubMed1993

Capsular type-specific polysaccharide partially inhibits group B Streptococcus-induced pulmonary hypertension.

Capsular type-specific polysaccharide is thought to be an important pathogenetic factor in Group B streptococcus (GBS) sepsis. To determine the effects of capsular type-specific polysaccharide on GBS-induced hemodynamic responses, anesthetized infant piglets were infused for 3 h with three related GBS Type lb strains that express different amounts of capsular type-specific polysaccharide. A larger capsule strain and a smaller capsule strain were isolated from an infected infant and its mother, respectively. A capsule-deficient mutant was then made from the larger capsule strain by transposon insertion mutagenesis. The smaller capsule strain and capsule-deficient mutant caused similar elevations in mean pulmonary artery pressure and pulmonary vascular resistance index and reductions in cardiac index. The larger capsule strain caused moderate pulmonary hypertension, but this response was smaller than for the other two GBS strains. Further comparisons in responses between the large capsule strain and its capsule-deficient mutant were then performed using unanesthetized piglets. The mutant caused significantly greater pulmonary hypertension and arterial plasma thromboxane B2 levels than the large capsule strain. The pulmonary hypertension induced by both strains was reversed by dazmegrel, a thromboxane A2 synthase inhibitor. These results suggest that (1) capsular type-specific polysaccharide is not an essential component in the generation of acute hemodynamic responses; (2) expression of large amounts of capsular type-specific polysaccharide on the organism surface partially inhibits GBS-induced pulmonary hypertension; and (3) the inhibition of the pulmonary responses is due to reduced thromboxane A2 release.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Bioadhesive properties of poly(alkylcyanoacrylate) nanoparticles coated with polysaccharide.

Development of bioadhesive nanoparticles is of great interest to improve drug absorption through the intestinal barrier. Various Polysaccharide-coated poly(alkylcyanoacrylate) nanoparticles were prepared. The bioadhesive properties of the nanoparticles coated with dextran or chitosan in end-on or side-on conformation were evaluated with an ex-vivo adsorption experiment on rat intestine. Results show that diffusion of nanoparticles in mucus layer was governed by the nanoparticle diameter and isotherms of adsorption were influenced by the nature of polysaccharide used. High amount of nanoparticles coated with chitosan can be entrapped in the mucus layer even at low nanoparticle concentration in suspension. When nanoparticle concentration increased, a pseudo-plateau was reached. In the case of dextran-coated nanoparticles, linear increase of adsorption was observed and no saturation phenomenon was highlighted over the range of nanoparticle concentration used in this study. These results suggested that interactions involved in bioadhesion mechanism depended on the nature of polysaccharide. Electrostatic interactions are enhanced between chitosan-coated nanoparticles and glycoproteins of mucus leading to a saturated adsorption phenomenon whereas dextran-coated nanoparticles interacted by non-electrostatic interactions with mucus resulting in a non-saturated phenomenon. Polysaccharides grafted at the nanoparticle surface in the brush conformation appeared more favorable to promote interactions of nanoparticles with glycoproteins of mucus in comparison with the more compact loop conformation of polysaccharide chains.

Adhesiveness↗