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Non-pathogenic bacteria are commonly eliminated by the host. Professional phagocytic cells of the immune system, such as macrophages and dendritic cells, recognize and by phagocytosis internalize microbes in specialized endocytic compartments called phagosomes. By fusing with endosomes, phagosomes mature, changing from an early to late state, and early and late endosomes differ in their external and internal biochemical composition. Then, fusion of late phagosomes with lysosomes leads to the formation of an acidic and degradative compartment, the phagolysosome, where bacteria are ultimately eliminated (Fairn and Grinstein, 2012). Bacterial pathogens have evolved several mechanisms to subvert the process of phagosome maturation and to survive and replicate in an intracellular niche that is protected from the immune response. Remarkably, distinct bacterial pathogens can be localized in similar endocytic compartments, suggesting they have a role in the control of the same endocytic steps. The biological machineries controlling endocytosis involve a variety of regulatory events in each step of intracellular membrane trafficking. Here, I would like to summarize and comment on all the discoveries on bacterial pathogens that control the localization or function of the small GTPases Rab5 and Rab7, and therefore modify the maturation from early to late phagosomes, because I believe such a transition is the best way to highlight how bacterial pathogens exploit the complexity of membrane trafficking to establish specific subversion mechanisms.

The complexity of Rab5 to Rab7 transition guarantees specificity of pathogen subversion mechanisms