Titlebook: Bacteria, Complement and the Phagocytic Cell; Felipe C. Cabello,Carla Pruzzo Conference proceedings 1988 Springer-Verlag Berlin Heidelberg

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Walter Leal Filho,Mark Mifsud,Rudi Pretorius of the mouse. As a first approach we asked whether relatively small differences in the quality of the cell surface 0 antigen of the bacteria would affect the outcome of the infection, and if so, by which mechanisms (Valtonen, 1970). This approach had the advantage that both the chemical structure a

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Education for Sustainability: A Wisdom Modeltial to generate bactericidal and opsonising activities. Most studies have investigated these activities in relationship to type b strains because of the importance of this serotype as a cause of life-threatening invasive infections in childhood. Anderson et al (1972) showed that either purified typ

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Shobha Sundaresan,Sushama Bavleare readily opsonized by complement through the alternate pathway (1) and as a result are rapidly ingested and killed by blood phagocytes. Surface M protein renders the organisms resistant to opsonization, ingestion and killing by phagocytic cells (2). Two hypotheses have been advanced to account fo

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Noah De Lissovoy,Raúl Olmo Fregoso Bailónace. Microorganisms resist elimination by attaching to components of the mucosal lining (1). The attachment can result from specific interactions of bacterial surface lectins with receptors consisting of oligosaccharide sequences in epithelial glycoconjugates (2).

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Capsular Polysaccharides (K Antigens) of ,,apsule is shown in Figure 1. It is easy to imagine that capsules protect the bacteria in inadvertent surroundings. They render the bacteria resistant to complement lysis and to phagocytosis and are, therefore, considered as virulence factors.