Bacterial agent host cells

This chapter will provide an overview of the research on anti-adhesion agents. Particular attention will be devoted to the anti-adherence agents derived from or foimd naturally in foods. In addition, the pathogen infection process, the architecture of host epithelial cell surfaces, and the chemistry and mechanisms involved in bacterial interactions with host cell surfaces will also be reviewed. 

Specific damage to bacteria is particularly practicable when a substance interferes with a metabolic process that occurs in bacterial but not in host cells. Clearly this applies to inhibitors of cell wall synthesis, because human and animal cells lack a cell wall. The points of attack of antibacterial agents are schematically illustrated in a grossly simplified bacterial cell, as depicted in (2). 

The final product must be free of adventitious agents that primarily include bacterial or viral pathogens and other biologic contaminates contributed during cell culture, such as DNA from prokaryotic or eukaryotic host cells and endotoxin. Purity testing for these factors must be performed throughout the production procedure and meet defined criteria before administration into humans. 

Because parasites are dependent on the host cell for nutrients and essential components, the arguments mentioned previously for alteration of the optimal metal concentration and its application to antibacterial and antiviral therapy are equally valid in the case of parasites. The sequestration of zinc and subsequent biochemical effects may present an example of this and the behaviour is somewhat reminiscent of the early and classic demonstration of the mode of action of 8-hydroxyquinoline (oxine). This reagent is also trypanocidal and, as with bacterial systems, cobalt protects against the lethal action [88]. The mode of action of oxine is presumably the same as for bacteria (see Chapter 9). Other chelating agents studied in... 

Only rifampicin can prevent the development of pox viruses at concentrations completely harmless for the host cell The mechanism of action of rifampicin on these large DNA viruses is now being studied and appears different from that on bacterial cells. This is an approach to specific antiviral chemotherapy and by now the rifampicin has been shown to exert its selective activity on some large DNA viruses (pox viruses and adenoviruses type I) and on the trachoma agent However, the rifampicin activity is limited it does not prevent the replication in mammalian cells of small DNA viruses nor the RNA viruses. 

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