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Review
. 2016 Feb;4(1):10.1128/microbiolspec.VMBF-0014-2015.
doi: 10.1128/microbiolspec.VMBF-0014-2015.

Contrasting Lifestyles Within the Host Cell

Elizabeth Di Russo Case  1 , James E Samuel  1
Affiliations
Review

Contrasting Lifestyles Within the Host Cell

Elizabeth Di Russo Case et al. Microbiol Spectr. 2016 Feb.

Abstract

Intracellular bacterial pathogens have evolved to exploit the protected niche provided within the boundaries of a eukaryotic host cell. Upon entering a host cell, some bacteria can evade the adaptive immune response of its host and replicate in a relatively nutrient-rich environment devoid of competition from other host flora. Growth within a host cell is not without their hazards, however. Many pathogens enter their hosts through receptor-mediated endocytosis or phagocytosis, two intracellular trafficking pathways that terminate in a highly degradative organelle, the phagolysosome. This usually deadly compartment is maintained at a low pH and contains degradative enzymes and reactive oxygen species, resulting in an environment to which few bacterial species are adapted. Some intracellular pathogens, such as Shigella, Listeria, Francisella, and Rickettsia, escape the phagosome to replicate within the cytosol of the host cell. Bacteria that remain within a vacuole either alter the trafficking of their initial phagosomal compartment or adapt to survive within the harsh environment it will soon become. In this chapter, we focus on the mechanisms by which different vacuolar pathogens either evade lysosomal fusion, as in the case of Mycobacterium and Chlamydia, or allow interaction with lysosomes to varying degrees, such as Brucella and Coxiella, and their specific adaptations to inhabit a replicative niche.

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Figures

Fig 1
Fig 1. Endosomal trafficking is coordinated by exchanges of lipids and Rab-GTPases
The normal endosomal pathway is illustrated here with major regulatory factors highlighted at each step. After uptake of a cargo, the phagosome fuses with early endosomes, acquiring Rab5, its effector EEA1, and VPS34, which coordinate the change in lipid profile of the endosomal membrane. Soon after, the compartment fuses with late endsomes, and Rab5 is exchanged for Rab7 and its effector RILP. LAMP and v-ATPases are also characteristic of the late endosome. Finally, the late endosome fuses with lysosomes, at which point the compartment is fully matured and highly degradative.
Fig 2
Fig 2. Intracellular pathogens have evolved distinct trafficking pathways to arrive within their ideal replicative niche
Intracelluar trafficking pathways are shown for Mycobacterium tuberculosis (Mtb), Chlamydia (Chl), Brucella (Br), and Coxiella burnetii (Cb). Key regulatory factors, such as Rab-GTPases, lipids, and bacterial factors are shown. Mtb fuses with early endosomes (EE), but inhibits fusion with late endosomes (LE), and replicates in a compartment (MCP) that is stalled at an early point along the endocytic pathway. Chl traffics away from the endosomal pathway, and escapes to replicate in a Golgi-associated Inclusion. Br allows EE and LE fusion as well as limited lysosomal fusion before trafficking to the ER to replicate in rBCVs (replicative Brucella containing vacuoles). Cb interacts with EE, autophagosomes, LE, and allows lysosomal fusion to arrive in the CCV (Coxiella containing vacuole), which resembles a terminal phagolysosome.
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References

    1. Fredlund J, Enninga J. Cytoplasmic access by intracellular bacterial pathogens. Trends in Microbiology. 2014;22:128–137. - PubMed
    1. Gomes LC, Dikic I. Autophagy in antimicrobial immunity. Molecular Cell. 2014;54:224–233. - PubMed
    1. Kinchen JM, Ravichandran KS. Phagosome maturation: going through the acid test. Nature Reviews. Molecular Cell Biology. 2008;9:781–795. - PMC - PubMed
    1. Vieira OV, Botelho RJ, Rameh L, Brachmann SM, Matsuo T, Davidson HW, Schreiber A, Backer JM, Cantley LC, Grinstein S. Distinct roles of class I and class III phosphatidylinositol 3-kinases in phagosome formation and maturation. The Journal of Cell Biology. 2001;155:19–25. - PMC - PubMed
    1. Di Paolo G, De Camilli P. Phosphoinositides in cell regulation and membrane dynamics. Nature. 2006;443:651–657. - PubMed

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