Surface capsular polysaccharides

Haemophilus influenzae immunoglobulins Human Antibodies raised against surface capsular polysaccharide of Haemophilus influenzae... 

Vaccines can be roughly categorized into killed vaccines and Hve vaccines. A killed vaccine can be (/) an inactivated, whole microorganism such as pertussis, (2) an inactivated toxin, called toxoid, such as diphtheria toxoid, or (J) one or more components of the microorganism commonly referred to as subunit vaccines. The examples are capsular polysaccharide of Streptococcus pneumoniae and the surface antigen protein for Hepatitis B vims vaccine. 

Studies on the white clover -Rhizobium trifolii interaction are the most advanced. Trifoliin A, a lectin present in clover-seedling roots, binds hapten reversibly to carbohydrate antigens cross-reactive on the capsular polysaccharide of R. trifolii and clover epidermal-cells.244 A specific hapten that inhibits binding of trifoliin A to both surfaces is 2-deoxy-D-arabino-hexose.245 It has also been shown that levels of trifoliin A on root hairs decline with increasing concentrations of nitrate, in parallel to root-nodule development,246 and that lectin receptors are transient on R. trifolii, in a way coinciding with its capacity to be adsorbed to clover roots.247... 

The importance of capsular polysaccharides in the immune response to bacterial infection is due to their location on the outer surface of the bacteria. They are at the interface of the many host-bacte-... 

The initial event in the pathogenesis of most bacterial infections is the attachment of the bacteria to the mucosal surface. This probably occurs by a receptor mechanism that exhibits a high degree of cellular specificity. Capsular polysaccharides have not been implicated in this... 

Attachment of capsular polysaccharides to the cell surface. Gram-negative CPS are attached to the outer membrane while Gram-positive CPS are attached to peptidoglycan or anchored in the inner membrane... 

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]. 

The 220 kDa cell-wall associated protein Sspl, which is organised in a fimbria-like structure, mediates attachment to polystyrene in an S. epidermidis strain [18,19] but has not been further studied. In addition, a capsular polysaccharide adhesin, PS/A, has been identified in S. epidermidis RP62A [35], This mediates primary attachment to unmodified silastic catheter surfaces, but not to other types of polymers such as polyethylene [36], Later studies have shown that PS/A is structurally very similar if not identical to polysaccharide intercellular adhesin (PIA) of S. epidermidis [37 12], This will be discussed in more detail in the next section of this review. 

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