Bacterial cell polysaccharide capsule

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. 

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. 

Capsules and capsular antigens are considered to be outer envelope polymers, usually high-molecular-weight acidic polysaccharides, which surround the bacterial cell in the form of a hydrophilic gel. Polysaccharides adhering weakly to the cell are known as slime layers. 

Biotechnological methods of hyaluronan production from bacterial strains involve cultivation in selected conditions where the polysaccharide capsule is formed during the stage of logarithmic growth on the surface of the bacterial cells. But at the stationary growing stage, HA can move into the cultural liquid and a capsule could become thin or disappears completely [30]. At the end of the process, up to 1-6 g of the desirable product could accumulate in 11 of the cultural liquid. HA accumulation could be controlled by the measurements of the viscosity of the cultural liquid. 

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]. 

Acetobacter xylinum produces two forms of cellulose (1) cellulose I, the rib-bon-like polymer, and (2) cellulose II, the thermodynamically more stable amorphous polymer [9]. They can be divided according to their morphological localization as intracellular polysaccharides located inside, or as part of the cytoplasmic membrane cell wall polysaccharides forming a structural part of the cell wall and extracellular polysaccharides located outside the cell wall. Extracellular polysaccharides occur in two forms loose slime, which is non-adherent to the cell and imparts a sticky consistency to bacterial growth on a solid medium or an increased viscosity in a liquid medium and microcapsules or capsules, which adhere to the ceU wall. 

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. 

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