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Bacteria bacterial adhesion

The first is glycosaminoglycan, a compound produced by the body that coats the epithelial cells of the bladder. This compound essentially separates the bladder from the urine by forming a protective layer against bacterial adhesion.14 A second compound known as Tamm-Horsfall protein is secreted into the urine, and prevents E. coli from binding to receptors present on the surface of the bladder. Other factors implicated in contributing to host defense mechanisms include immunoglobulins, specifically IgA, and lactobacilli, bacteria that are part of the normal vaginal flora.13,15... [Pg.1153]

Relation between bacterial adhesion to sulphated polystyrene (A) and cell surface characteristics as determined by electrophoretic mobility and contact angle measurement. Results were obtained by interpolating the data points for the adhesion of 17 different strains of bacteria. [Pg.281]

To measure the adhesion strength of bacteria, it is necessary to remove them from the surface. Weiss (1961) measured bacterial adhesion by allowing cells to settle onto a glass surface of a sealed chamber, and then counting them with the aid of a microscope. After a period of incubation the chamber was turned upside down, the unattached cells fell from the surface and the remaining attached cells were recounted. This adhesion number method is purely observational, as it does not measure adhesion directly. Weiss also described a disc-shearing device,... [Pg.72]

Fig. 9 Example of a contact-killing and microbe-repelling surface, (a) Antimicrobial cationic polyW.iV-dimethyl-iVTethoxycarbonylmethyll-iV-P -tniethacryloyloxylethyll-ammonium bromide) left structure) effectively kills bacteria, (b) The polymer is converted into the corresponding nonfouling zwitterionic derivative (right structure) upon hydrolysis, (c) Dead bacteria remaining on the surface are repelled from the nonfouling surface, (d) The zwitterionic surface itself is highly resistant to bacterial adhesion. Reproduced and adapted from [136]... Fig. 9 Example of a contact-killing and microbe-repelling surface, (a) Antimicrobial cationic polyW.iV-dimethyl-iVTethoxycarbonylmethyll-iV-P -tniethacryloyloxylethyll-ammonium bromide) left structure) effectively kills bacteria, (b) The polymer is converted into the corresponding nonfouling zwitterionic derivative (right structure) upon hydrolysis, (c) Dead bacteria remaining on the surface are repelled from the nonfouling surface, (d) The zwitterionic surface itself is highly resistant to bacterial adhesion. Reproduced and adapted from [136]...
First, bacterial adhesion (usually gram-positive cocci and filamentous bacteria) occurs primarily through a Ca + complex formation between carboxyl (COO ) and phosphate (HPOs ) groups of bacterial surface and acquired pelhcle, although van der Waals forces and repulsive electrostatic forces are also present. Some specific bacterial surface proteins also serve as adhesins for specific receptors on acquired peUicle. Pellicle-integrated immunoglobulins also bind bacteria specifically. [Pg.2058]

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]. [Pg.1588]

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]. [Pg.1590]

Bacteria are simple unicellular organisms that constantly grow. They have a membrane and cell wall. Fimbriae are especially important for bacterial adhesion, a critical factor in dental disease development. Lipopolysaccharide is a covalent lipid and polysaccharide structure that contains unusual saccharides and fatty acids. The lipid is at one end and inserts it into the plasma membrane. LPS is invariably recognized as foreign by receptors on mammalian cells that recognize the unique structure and activate inflammation such as gingivitis. [Pg.16]

The examples discussed above impressively show the diversity and importance of interaction between bacterial adhesion determinants and carbohydrate-containing receptor molecules. Pathogenic bacteria use binding to carbohydrates in different disease stages. However, many questions remain to be answered to unravel the full spectrum of bacteria-host interactions via carbohydrate binding. [Pg.116]

Bacterial Adhesion. Bacteria often adhere to interfaces and the resulting biofilms can cause a nuisance on ship hulls, to water reticulation and hydro-electric pipelines and in heat exchangers... [Pg.177]


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Bacterial adhesion

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