Listeriosis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
''Listeria'' uses the cellular machinery to move around inside the host cell: it induces directed polymerization of [[actin]] by the ActA [[transmembrane protein]], thus pushing the bacterial cell around. | |||
''Listeria'' ''monocytogenes'' for example, encodes virulence genes which are thermoregulated. The expression of virulence factor is optimal at 37 degrees Celsius and is controlled by a transcriptional activator, PrfA, whose expression is thermoregulated by the [[PrfA thermoregulator UTR]] element. At low temperatures, the PrfA transcript is not translated due to [[Cis-regulatory element|structural elements]] near the ribosome binding site. As the bacteria infects the host, the temperature of the host melts the structure and allows translation initiation for the virulent genes. | |||
==Pathogenesis== | ==Pathogenesis== | ||
''L monocytogenes'' is ubiquitous in the environment. The main route of acquisition of ''Listeria'' is through the ingestion of contaminated food products. ''Listeria'' has been isolated from raw meat, dairy products, vegetables, and seafood. Soft cheeses and unpasteurized milk are potential dangers, however post-[[pasteurization]] outbreaks of infection from dairy have been from pasteurized milk. | ''L monocytogenes'' is ubiquitous in the environment. The main route of acquisition of ''Listeria'' is through the ingestion of contaminated food products. ''Listeria'' has been isolated from raw meat, dairy products, vegetables, and seafood. Soft cheeses and unpasteurized milk are potential dangers, however post-[[pasteurization]] outbreaks of infection from dairy have been from pasteurized milk. | ||
==Mechanism of Infection== | |||
The majority of ''Listeria'' bacteria are targeted by the [[immune system]] before they are able to cause [[infection]]. Those that escape the immune system's initial response, however, spread though intracellular mechanisms and are therefore guarded against circulating immune factors (AMI). | |||
: | To invade, ''Listeria'' induces macrophage [[phagocytosis|phagocytic]] uptake by displaying D-galactose receptors that are then bound by the [[macrophage]]'s [[polysaccharide]] receptors (Notably, in most bacterial infections it is the host cell, not the bacteria, that displays the polysaccharide). Once phagocytosed, the bacteria is encapsulated by the host cell's acidic phagolysosome organelle. ''Listeria'', however, escapes the phagolysosome by lysing the vacuole's entire membrane with secreted hemolysin, <ref name="rtsjournal1">{{cite journal | quotes=no |author= Tinley, L.G. et al |year=1989|url=http://www.jcb.org/cgi/reprint/109/4/1597|title= Actin Filaments and the Growth, Movement, and Spread of the Intracellular Bacterial Parasite, ''Listeria monocytogenes'' |journal=The Journal of Cell Biology |volume=109 |pages=1597-1608}}</ref> now characterized as the exotoxin [[listeriolysin O]]. The bacteria then replicate inside the host cell's cytoplasm. | ||
''Listeria'' must then navigate to the cell's periphery to spread the infection to other cells. Outside of the body, ''Listeria'' has [[flagella]]r-driven motility. However, at 37°C, flagella cease to develop and the bacteria instead usurps the host cell's [[cytoskeleton]] to move. ''Listeria'', inventively, polymerizes an [[actin]] tail or "comet" , using host-produced actin filaments <ref name="rts4">{{cite web | |||
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| title =Listeria | |||
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| publisher =MicrobeWiki.Kenyon.edu | |||
| date = 16 August 2006 | |||
| url =http://microbewiki.kenyon.edu/index.php?title=Listeria&oldid=5472 | |||
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| accessdate = 2007-03-07 }}</ref> with the promotion of virulence factor ActA. The comet forms in a polar manner <ref name="rtsjournal2">{{cite journal | quotes=no |author= Laine, R.O. et al |year=1998|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=108414|title= Gelsolin, a Protein That Caps the Barbed Ends and Severs Actin Filaments, Enhances the Actin-Based Motility of Listeria monocytogenes in Host Cells |journal=Infection and Immunity |volume=66(8) |pages=3775-3782}}</ref> and aids the bacteria's migration to the host cell's outer membrane. Gelsolin, an actin filament severing protein, localizes at the tail of ''Listeria'' and accelerates the bacterium's motility. Once at the cell surface, the actin-propelled ''Listeria'' pushes against the cell's membrane to form protrusions called [[filopod]]s or "rockets". The protrusions are guided by the cell's leading edge <ref name="rtsjournal3">{{cite journal | quotes=no |author= Galbraith, C.G. et al |year=2007|url= |title= Polymerizing Actin Fibers Position Integrins Primed to Probe for Adhesion Sites |journal=Science |volume=315 |pages=992-995}}</ref>to contact adjacent cells which subsequently engulf the ''Listeria'' rocket and the process is repeated, perpetuating the infection. Once phagocytosed, the ''Listeria'' is never again extracellular: it is an intracytoplasmic parasite like ''[[Shigella flexneri]]'' and ''[[Rickettsia]]''. | |||
==References== | ==References== | ||
Revision as of 15:39, 9 February 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Listeria uses the cellular machinery to move around inside the host cell: it induces directed polymerization of actin by the ActA transmembrane protein, thus pushing the bacterial cell around.
Listeria monocytogenes for example, encodes virulence genes which are thermoregulated. The expression of virulence factor is optimal at 37 degrees Celsius and is controlled by a transcriptional activator, PrfA, whose expression is thermoregulated by the PrfA thermoregulator UTR element. At low temperatures, the PrfA transcript is not translated due to structural elements near the ribosome binding site. As the bacteria infects the host, the temperature of the host melts the structure and allows translation initiation for the virulent genes.
Pathogenesis
L monocytogenes is ubiquitous in the environment. The main route of acquisition of Listeria is through the ingestion of contaminated food products. Listeria has been isolated from raw meat, dairy products, vegetables, and seafood. Soft cheeses and unpasteurized milk are potential dangers, however post-pasteurization outbreaks of infection from dairy have been from pasteurized milk.
Mechanism of Infection
The majority of Listeria bacteria are targeted by the immune system before they are able to cause infection. Those that escape the immune system's initial response, however, spread though intracellular mechanisms and are therefore guarded against circulating immune factors (AMI).
To invade, Listeria induces macrophage phagocytic uptake by displaying D-galactose receptors that are then bound by the macrophage's polysaccharide receptors (Notably, in most bacterial infections it is the host cell, not the bacteria, that displays the polysaccharide). Once phagocytosed, the bacteria is encapsulated by the host cell's acidic phagolysosome organelle. Listeria, however, escapes the phagolysosome by lysing the vacuole's entire membrane with secreted hemolysin, [1] now characterized as the exotoxin listeriolysin O. The bacteria then replicate inside the host cell's cytoplasm.
Listeria must then navigate to the cell's periphery to spread the infection to other cells. Outside of the body, Listeria has flagellar-driven motility. However, at 37°C, flagella cease to develop and the bacteria instead usurps the host cell's cytoskeleton to move. Listeria, inventively, polymerizes an actin tail or "comet" , using host-produced actin filaments [2] with the promotion of virulence factor ActA. The comet forms in a polar manner [3] and aids the bacteria's migration to the host cell's outer membrane. Gelsolin, an actin filament severing protein, localizes at the tail of Listeria and accelerates the bacterium's motility. Once at the cell surface, the actin-propelled Listeria pushes against the cell's membrane to form protrusions called filopods or "rockets". The protrusions are guided by the cell's leading edge [4]to contact adjacent cells which subsequently engulf the Listeria rocket and the process is repeated, perpetuating the infection. Once phagocytosed, the Listeria is never again extracellular: it is an intracytoplasmic parasite like Shigella flexneri and Rickettsia.
References
- ↑ Tinley, L.G.; et al. (1989). "Actin Filaments and the Growth, Movement, and Spread of the Intracellular Bacterial Parasite, Listeria monocytogenes". The Journal of Cell Biology. 109: 1597–1608. Unknown parameter
|quotes=ignored (help) - ↑ "Listeria". MicrobeWiki.Kenyon.edu. 16 August 2006. doi:. Check
|doi=value (help). Retrieved 2007-03-07. - ↑ Laine, R.O.; et al. (1998). "Gelsolin, a Protein That Caps the Barbed Ends and Severs Actin Filaments, Enhances the Actin-Based Motility of Listeria monocytogenes in Host Cells". Infection and Immunity. 66(8): 3775–3782. Unknown parameter
|quotes=ignored (help) - ↑ Galbraith, C.G.; et al. (2007). "Polymerizing Actin Fibers Position Integrins Primed to Probe for Adhesion Sites". Science. 315: 992–995. Unknown parameter
|quotes=ignored (help)