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Chapter category: Bacterial Virulence

Evasion of Phagosome Lysosome Fusion and Establishment of a Replicative Organelle by the Intracellular Pathogen Legionella pneumophila

This chapter appears in the following book:

Intracellular Pathogens in Membrane Interactions and Vacuole Biogenesis

Edited by: Jean-Pierre Gorvel
ISBN: 0-306-47833-1
» Get more information about this book at landesbioscience.com «

Chapter authors:
Craig R. Roy and Jonathan C. Kagan


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Most human pathogens that survive and proliferate in normally sterile environments have evolved specialized virulence determinants that facilitate evasion of host defense mechanisms. Microbial strategies to evade host immunity are often geared towards professional phagocytes. This is because macrophages are always on the lookout for bacteria that have breached physical barriers to gain access to a privileged site. When foreign invaders are encountered, they are usually engulfed by macrophages and then destroyed when the phagosomes in which they reside are delivered to lysosomes. To avoid destruction, many microbial pathogens modulate vesicle trafficking in eukaryotic host cells in order to prevent phagosome lysosome fusion. Although many microbial pathogens have the ability to alter phagosome trafficking, it is unclear how most of them accomplish this feat. Legionella pneumophila are bacteria that have the ability to alter maturation of the endocytic vacuole in which they reside initially, allowing them to establish an organelle within phagocytic host cells that supports replication. Rather than fusing sequentially with early endosomes, late endosomes, then lysosomes; phagosomes containing L. pneumophila will associate rapidly with smooth vesicles and are remodeled into unique organelles decorated with ribosomes. Genetic analysis has revealed that a type IV-related secretion system is required by L. pneumophila to control phagosome biogenesis. It is believed that L. pneumophila use this specialized secretion system during uptake to inject proteins into the host cell. Proteins delivered into the host cell by L. pneumophila would then act on host factors that regulate vesicle trafficking. In theory, L. pneumophila could prevent phagosome maturation by either inhibiting the function of host factors required for trafficking of endocytic vesicles or they could promote rapid remodeling of the endocytic vacuole through subverting factors used for biogenesis of other cellular organelles. Recent evidence suggests that L. pneumophila may employ a combination of both strategies. Although the effector proteins being injected into host cells have not been identified, we propose that L. pneumophila use a type-IV related secretion system to deliver one set of effectors that will inhibit endocytic maturation momentarily, and then intracellular bacteria remodel their endocytic vacuole using a second set of effectors that subvert host factors used for biosynthetic transport. This allows L. pneumophila to create a specialized organelle that shares many features with the host cell endoplasmic reticulum.

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