ISOLATION AND CHARACTERIZATION OF PATHOGEN-CONTAINING PHAGOSOMES

Publisher Summary The chapter illustrates a range of techniques to study the phagosome-differentiation mechanisms for model systems, such as IgG-coated latex particles and for the pathogens Leishmania and Mycobacterium . Different intracellular pathogens exploit different locations to sustain their infection. Despite the obvious perils of the host cell lysosomal system many pathogens remain inside their phagosome. Both the protozoan parasite Leishmania and the bacterial pathogen Mycobacterium enter their host macrophage by phagocytosis and remain intravacuolar throughout their intracellular infection. Their strategies of phagosome modulation are diametrically opposite. Leishmania actively enhances the interchange between its vacuole and the host cell's endosomal network, whereas Mycobacterium inhibits fusion of its vacuole with endosomal vesicles. These functional differences facilitate a comparative approach to the identification of pathogen-specific modulation of their phagosome. Both pathogens overcome these short-term problems, procure an adequate supply of nutrients, and prevent their host cell from inducing a protective immune response.