Bacterial capsule polysaccharides

In 1944, Avery, MacLeod, and McCarty [85] extracted highly polymerized deoxypentose nucleic acid from the active preparation and demonstrated that this purified DNA could transform the R cell into an S cell. Later, transformation was demonstrated with a variety of bacteria, including E. coli, Shigella parody sent erica, Bacillus proteus, Salmonella, staphylococci, tubercular bacilli, and other bacteria. Mutations induced by transforming agents cause molecular changes in the elaboration of the bacterial capsule polysaccharide, in the appearance or disappearance of enzymes, and in the development or resistance to antibiotics. 

Pneumococcal— These polysaccharides control the immunological type specificity of the pneumococci by their presence in the bacterial capsule. Their constituents are D-glucose, D-glucuronic add, aldobionic adds and amino sugars. The proportions of each vary from one type to another and certain constituents may be missing. 

Most bacterial capsules are polysaccharides with a specific structure. In many respects, the capsular polysaccharide can be considered an identifying feature of the organism. The pneumococci are divided into types (or groups) that are defined by a particular immunological precipitin reaction of the capsular polysaccharide with an antibody preparation obtained by inoculation of the polysaccharide into an animal host such as a rabbit. The reaction is usually highly specific and depends on the structure of the polysaccharide. S. pneumoniae has been found to have over 80 different immunological types and, therefore, 80 different polysaccharide structures. 

Polysaccharides occur (1) in cell walls, (2) extracellularly in capsules and gums, and (3) inside of bacterial cells. The first two have already been discussed. 

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. 

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... 

These bacterial polysaccharides have been considered to be slimes they are often in reality loose capsules that are produced extracellularly by the bacteria. It was found that low molecular weight L. mesenteroides NRRL B-512F dextran could be used as a blood plasma extender and was produced on a relatively large scale during the cold war , but also found uses as a gel-filtration material when cross-linked by epichlorohydrin to give a family of cross-linked dextrans [41]. 

Capsular and extracellular polysaccharides are involved in several aspects of cellular behavior that are tied to bacterial survival and virulence [321]. The capsule layer provides a physical barrier that prevents the bacteria from drying out, aiding in survival outside a host. CPS are also involved in colonization and biofilm formation. In some bacteria CPS promote adherence to surfaces, aiding colonization and biofilm formation, while CPS in other bacteria inhibit adhesion and biofilm formation [344]. 

In both S. pneumoniae and N. meningitidis, the thickness of the capsule has been shown to vary at different points in infection. In Neisseria meninigitidis decreased capsule production enhances tissue invasion, while increased capsule production is essential for survival in systemic infections [349]. Likewise, studies in pneumococci have suggested that the capsule prevents bacterial adhesion to epithelial cells, as well as to endothelial cells [350,351,352]. Bacteria producing less capsular polysaccharide more efficiently colonize mucosal surfaces, while those producing more capsule are more virulent in systemic infections [350,353]. 

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). 

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. 

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