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Chapter 24 : , a Pathogen of Amoebae and Macrophages

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Abstract:

Most species, including , are aquatic microbes; other species thrive in soil. There, the microbe naturally infects amoebae and protozoa, but, when given the opportunity, can infect human alveolar macrophages and cause the severe pneumonia Legionnaires’ disease. In particular, the phagosomal transporter protein A (PhtA) enables intracellular bacteria to acquire threonine from macrophages and amoebae, whereas PhtJ behaves as a valine transporter, and PhtC and PhtD are critical for thymidine assimilation. In some manner, the secreted proteins promote growth of in amoebae, macrophages derived from human peripheral blood, and the lungs of A/J mice, as judged by comparing the yield of type II secretion-competent with corresponding mutants. The prevailing concept holds that, to replicate in macrophages, intercepts vesicular traffic from the secretory pathway. For example, in the absence of RalF or SidM, nevertheless replicates efficiently in amoebae and macrophages. Moreover, when compared with restrictive C57Bl/6 mouse macrophages, permissive A/J naip5 macrophages that are subjected to amino acid starvation exhibit markedly slower maturation of autophagosomes. In the absence of SdhA, induces mitochondrial damage, caspase activation, and cell death of A/J mouse macrophages, and the intracellular mutant bacteria cannot replicate. Like SdhA, SidH contributes to growth in mouse macrophages, but not human monocytic cells or . After ingestion by macrophages, encounters multiple arms of the innate immune system.

Citation: Swanson M, Bryan A. 2009. , a Pathogen of Amoebae and Macrophages, p 393-403. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch24

Key Concept Ranking

Type IV Secretion Systems
0.42644653
Type II Secretion System
0.4142478
Bacterial Proteins
0.4104201
0.42644653
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Image of FIGURE 1
FIGURE 1

is an environmental bacterium that causes opportunistic infections of humans. is transmitted to humans by the respiratory route from water or soil that harbors its natural hosts, amoebae and protozoa. In the absence of a robust cellmediated immune response, the bacteria can replicate in alveolar macrophages and cause the severe pneumonia, Legionnaires’ disease.

Citation: Swanson M, Bryan A. 2009. , a Pathogen of Amoebae and Macrophages, p 393-403. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch24
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Image of FIGURE 2
FIGURE 2

Metabolic cues govern the life cycle. In macrophages and broth, the bacterium responds to metabolic cues by alternating between a replicative form and a cell type equipped for transmission to a new host. After phagocytosis, the bacteria rely on Pht proteins to acquire essential metabolites. When amino acids become scarce or fatty acid biosynthesis is strained, the enzymes RelA or SpoT, respectively, generate (p)ppGpp, a second messenger that coordinates the bacterium’s exit from logarithmic phase with the expression of multiple transmission traits, including cytotoxicity, motility, osmotic resistance, motility, and the capacity to inhibit phagosome-lysosome fusion.

Citation: Swanson M, Bryan A. 2009. , a Pathogen of Amoebae and Macrophages, p 393-403. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch24
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Image of FIGURE 3
FIGURE 3

Trafficking of in macrophages derived from bone marrow of A/J mice. After phagocytosis, evades immediate delivery to lysosomes. Instead, its vacuole acquires membranes from the secretory pathway and also several features typical of autophagosomes. Once the bacterium differentiates to the replicative form, its vacuole slowly merges with the lysosomal compartment, where replication continues. How quickly and extensively the replication vacuole interacts with the endosomal compartment depends on the host cell. For example, macrophages from resistant C57Bl/6 mice rapidly deliver to lysosomes, whereas permissive human macrophages derived from peripheral blood monocytes harbor replicating within a compartment derived from ER. See text for details.

Citation: Swanson M, Bryan A. 2009. , a Pathogen of Amoebae and Macrophages, p 393-403. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch24
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Image of FIGURE 4
FIGURE 4

The type IV secretion system provides a conduit to the host cytoplasm. Composed of dozens of proteins encoded by the and genes, the secretion apparatus spans the inner and outer membranes. A pilus may contact the host plasma membrane. Three Dot proteins have been shown or are predicted to hydrolyze ATP; these may drive the assembly of the complex or regulate its activity. Substrates of the apparatus are thought to rely on particular adaptor proteins for their delivery. For details, see the text and .

Citation: Swanson M, Bryan A. 2009. , a Pathogen of Amoebae and Macrophages, p 393-403. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch24
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FIGURE 5

Mouse macrophages recognize cytosolic flagellin to restrict replication. Macrophages that encode the NOD-like receptor proteins Naip5 and Ipaf respond to flagellin of type IV secretion-competent bacteria by activating a cell death program mediated by caspase-1. As a consequence, the macrophages deny its replication niche while releasing the proinflammatory cytokines IL-1β and IL-18.

Citation: Swanson M, Bryan A. 2009. , a Pathogen of Amoebae and Macrophages, p 393-403. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch24
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References

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1. Bruggemann, H.,, C. Cazalet, and, C. Buchrieser. 2006a. Adaptation of Legionella pneumophila to the host environment, role of protein secretion, effectors and eukaryotic-like proteins. Curr. Opin. Microbiol. 9:8694.
2. Bruggemann, H.,, A. Hagman,, M. Jules,, O. Sismeiro,, M. A. Dillies,, C. Gouyette,, F. Kunst,, M. Steinert,, K. Heuner,, J. Y. Coppee, and, C. Buchrieser. 2006b. Virulence strategies for infecting phagocytes deduced from the in vivo transcriptional program of Legionella pneumophila. Cell. Microbiol. 8:12281240.
3. DebRoy, S.,, J. Dao,, M. Soderberg,, O. Rossier, and, N. P. Cianciotto. 2006. Legionella pneumophila type II secretome reveals unique exoproteins and a chitinase that promotes bacterial persistence in the lung. Proc. Natl. Acad. Sci. USA 103:1914619151.
4. Delbridge, L. M.,, and M. X. O’Riordan. 2007. Innate recognition of intracellular bacteria. Curr. Opin. Immunol. 19:1016.
5. Edelstein, P. H.,, and N. P. Cianciotto. 2005. Legionella, p. 2711–2724. In G. L. Mandell,, E. Bennett, and, R. Dolin (ed.), Principles and Practice of Infectious Diseases, 6th ed. Elsevier, Philadelphia, PA.
6. Fernandez-Moreira, E.,, J. H. Helbig, and, M. S. Swanson. 2006. Membrane vesicles shed by Legionella pneumophila inhibit fusion of phagosomes with lysosomes. Infect. Immun. 74:32853295.
7. Horwitz, M. A. 1983. Formation of a novel phagosome by the Legionnaires’ disease bacterium (Legionella pneumophila) in human monocytes. J. Exp. Med. 158:13191331.
8. Luo, Z. Q.,, and R. R. Isberg. 2004. Multiple substrates of the Legionella pneumophila Dot/Icm system identified by interbacterial protein transfer. Proc. Natl. Acad. Sci. USA 101:841846.
9. Molofsky, A. B.,, and M. S. Swanson. 2004. Differentiate to thrive: lessons from the Legionella pneumophila life cycle. Mol. Microbiol. 53:2940.
10. O’Conner, T. O.,, M. Heidtman, and, R. R. Isberg. 2008. Mechanisms of intracellular survival and replication of Legionella pneumophila, p. 181–211. In K. Heuner and, M. Swanson (ed.), Legionella Molecular Microbiology. Horizon Scientific Press, Norwich, United Kingdom.
11. Sexton, J. A.,, and J. P. Vogel. 2002. Type IVB secretion by intracellular pathogens. Traffic 3:178185.
12. Shohdy, N.,, J. A. Efe,, S. D. Emr, and, H. A. Shuman. 2005. Pathogen effector protein screening in yeast identifies Legionella factors that interfere with membrane trafficking. Proc. Natl. Acad. Sci. USA 102:48664871.
13. Swanson, M. S. 2006. Autophagy: eating for good health. J. Immunol. 177:49454951.
14. Tilney, L. G.,, O. S. Harb,, P. S. Connelly,, C. G. Robinson, and, C. R. Roy. 2001. How the parasitic bacterium Legionella pneumophila modifies its phagosome and transforms it into rough ER: implications for conversion of plasma membrane to the ER membrane. J. Cell Sci. 114:46374650.
15. Vincent, C. D.,, J. R. Friedman,, K. C. Jeong,, E. C. Buford,, J. L. Miller, and, J. P. Vogel. 2006. Identification of the core transmembrane complex of the Legionella Dot/Icm type IV secretion system. Mol. Microbiol. 62:12781291.
16. Vogel, J. P.,, H. L. Andrews,, S. K. Wong, and, R. R. Isberg. 1998. Conjugative transfer by the virulence system of Legionella pneumophila. Science 279:873876.

Tables

Generic image for table
TABLE 1

Effectors delivered by type IV secretion that target host pathways

Citation: Swanson M, Bryan A. 2009. , a Pathogen of Amoebae and Macrophages, p 393-403. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch24

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