Capsule, polysaccharide

Resistance to phagocytosis is sometimes associated with specific components of the cell wall and/or with the presence of capsules surrounding the cell wall. Classic examples of these are the M-proteins of the streptococci and the polysaccharide capsules of pneumococci. The acidic polysaccharide K-antigens of Escherichia coli and Sal typhi behave similarly, in that (i) they can mediate attachment to the intestinal epithelial cells, and (ii) they render phagocytosis more difficult. Generally, possession of an extracellular capsule will reduce the likelihood of phagocytosis. 

BraynerCoradin, T., Fievet-Vincent, F., Livage, J. and Fievet, F. (2005) Algal polysaccharide capsule-templated growth of magnetic nanoparticles. New Journal of Chemistry, 29,... 

A common characteristic of most CNS bacterial pathogens (e.g., H. influenzae, Escherichia coli, and N. meningitidis) is the presence of an extensive polysaccharide capsule that is resistant to neutrophil phagocytosis and complement opsonization. 

Clearly, further studies will be necessary to sort out the multiple factors involved in the in vivo immune response to C. neoformans carbohydrate-mimetic peptides. Several conclusions may be drawn from the results to date. Peptides that mimic the cryptococcal capsular polysaccharide show specificity, in that each peptide binds with differing affinity to closely related mAbs [140,149]. The pattern of binding to protective and nonprotective mAbs differs between the mimetic peptides and the polysaccharide [140]. Protective efficacy is related to the location of carbohydrate epitopes recognized by these mAbs, within the polysaccharide capsule, but hkely also depends on interactions between mAbs and cellular responses [149]. Peptides have been shown to be functional, immunogenic mimics, but their protective efficacy depends on multiple factors, including the type of Abs elicited and interactions with the cellular immune system. Protective efficacy does not correlate with binding affinity to representative mAbs, but rather depends on the nature of these interactions. 

Beta-lactam antibiotics must pass through the outer layer of the cell in order to get the desired PBP to the surface of the membrane. In Gram-positive bacteria, the cell membrane is the only layer covering the cytoplasmic membrane. In a few types of this bacteria, there is a polysaccharide capsule on the outer side of the cell membrane. However, not one of the described structures can serve as a barrier for the diffusion of small molecules such as beta-lactams. Therefore, the idea that the cause of possible resistance is the inability of beta-lactam antibiotics to get the desired PBP is not likely to be a possible mechanism of resistance for Gram-positive bacteria. 

Most slime-forming bacteria are aerobic. Species such as Pseudomonas produce an extracellular, gel-like, polysaccharide capsule which acts to protect and shield the organism. When in combination with other metabolic by-products, bacteria... 

H. J. Jennings Structure, conformation and immunology of the polysaccharide capsules of human pathogenic bacteria... 

That Cross-react with the Polysaccharide Capsules of Human Pathogenic Bacteria... 

The function of the polysaccharide capsule in inhibiting the alternative pathway is most satisfactorily and simply explained by the fact that it masks the underlying, bacterial structures (for example, tei-choic acids), which are known to be powerful activators of the alternative pathway.153-158 However, although this mechanism is no doubt... 

Although it has, to date, not been possible to identify any common structural feature among all the polysaccharide capsules of bacteria associated with the most pathogenic human disease, there is one common feature in many of them. The capsular polysaccharide of type III group B Streptococcus has terminal sialic acid residues in its structure,62,63 as do the groups B and C N. meningitidis and K1 E. coli.3 -34 The ability of terminal sialic acid residues to inhibit the activation of complement by way of the alternative pathway has been well docu-... 

Cryptococcus (19) none varied, but all use mi/o-inositol spherical, oval, or elongate budding-cells, usually with a polysaccharide capsule not filamentous 24,43... 

This chapter describes dental caries (tooth decay) and its causes. Sucrose and other mono- and disaccharides are metabolized to acid (lactate) by bacteria that remain in stagnation areas of the teeth. Rats and hamsters fed a 50% sucrose diet developed a caries-sensitive, predominantly gram-positive microbiota that became caries resistant when the rodents were fed penicillin (Sect. 1). Further studies identified Streptococcus mutans (S. mutans) as the etiological agent. This organism synthesizes an insoluble polysaccharide capsule that is stable and retains lactate at the enamel surface (Sect. 2). The key enzyme, glucosyl transferase, is related to salivary amylase which adheres to oral bacteria and enhances bacterial acid production. The chapter concludes with a discussion of salivary and other factors responsible for the marked variation observed in individual caries experience (Sect. 3). 

On-the-fly comparison of two gene clusters from Streptococcus pneumoniae for the biosynthesis of differing polysaccharide capsule structures. Sequences will be selected from the public databases for the generation of comparison files and subsequent visualization in ACT. 

The example describes the creation of a comparison between two entries uploaded into WebACT from the public DNA database. Each entry contains the DNA sequence and annotation for a gene cluster from S. pneumoniae encoding the biosynthesis of a particular polysaccharide capsule structure. Each strain of S. pneumoniae carries 1 version of the gene cluster out of a possible 90 (17). The different capsule types are conventionally determined by serotyping. The capsule forms the outer coating of these bacterial cells and differences in their structure affect interactions with the human host. 

Prevnar is a glycoconjugate heptavalent pneumococcal vaccine for young children made from the polysaccharide capsule of the pneumococcus (20). Although older vaccines made from pneumococcus capsular polysaccharide are available for adults, young children cannot make antibodies to the capsule. By coupling the pneumococcal capsular polysaccharide with a protein carrier, a vaccine was created that will trigger an infant s immune system to produce antibodies. 

Avery wanted to be certain that the active agent was the DNA and not a small amount of protein contamination. To verify the result, a quantity of DNase, an enzyme that would destroy the DNA without affecting the protein, was prepared and added to the sample. When a portion of bacteria was tested, it could no longer transform the unencapsulated bacteria into encapsulated bacteria. Avery and his co-workers had conclusively proven that DNA was the transforming principle responsible for the development of polysaccharide capsules in the tmencapsulated bacteria. 

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