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Contrasting Lifestyles Within the Host Cell

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  • Authors: Elizabeth Di Russo Case1, James E. Samuel2
  • Editors: Indira T. Kudva3, John P. Bannantine4
    Affiliations: 1: Department of Microbial Pathogenesis and Immunology, College of Medicine, Texas A&M Health Sciences Center, Bryan, TX 77807; 2: Department of Microbial Pathogenesis and Immunology, College of Medicine, Texas A&M Health Sciences Center, Bryan, TX 77807; 3: National Animal Disease Center, Agricultural Research Service, U.S. Department of Agriculture, Ames, IA; 4: National Animal Disease Center, Agricultural Research Service, U.S. Department of Agriculture, Ames, IA
  • Source: microbiolspec February 2016 vol. 4 no. 1 doi:10.1128/microbiolspec.VMBF-0014-2015
  • Received 17 March 2015 Accepted 26 May 2015 Published 26 February 2016
  • James E. Samuel, [email protected]
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  • 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 , , , and , 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 and , or allow interaction with lysosomes to varying degrees, such as and , and their specific adaptations to inhabit a replicative niche.

  • Citation: Case E, Samuel J. 2016. Contrasting Lifestyles Within the Host Cell. Microbiol Spectrum 4(1):VMBF-0014-2015. doi:10.1128/microbiolspec.VMBF-0014-2015.


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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 , , , and , 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 and , or allow interaction with lysosomes to varying degrees, such as and , and their specific adaptations to inhabit a replicative niche.

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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 endosomes, 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.

Source: microbiolspec February 2016 vol. 4 no. 1 doi:10.1128/microbiolspec.VMBF-0014-2015
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Intracellular pathogens have evolved distinct trafficking pathways to arrive within their ideal replicative niche. Intracellular trafficking pathways are shown for (Mtb), (Chl), (Br), and (Cb). Key regulatory factors, such as Rab-GTPases, lipids, and bacterial factors are shown. sis 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 -containing vacuoles). Cb interacts with EE, autophagosomes, and LE and allows lysosomal fusion to arrive in the CCV (-containing vacuole), which resembles a terminal phagolysosome.

Source: microbiolspec February 2016 vol. 4 no. 1 doi:10.1128/microbiolspec.VMBF-0014-2015
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