June 10, 2013 at 4:44 am #3301
nfect Immun. 2013 Jun 3. [Epub ahead of print]
[h=1]The Gallbladder Epithelium as a Niche for Chronic Salmonella Carriage.[/h]Gonzalez-Escobedo G, Gunn JS.
[h=3]Source[/h]Center for Microbial Interface Biology.
Although typhoid fever has been intensively studied, chronic typhoid carriage still represents a problem for the transmission and persistence of the disease in endemic areas. This chronic state is highly associated with the presence of gallstones in the gallbladder of infected carriers upon which Salmonella can form robust biofilms. However, we hypothesize that in addition to gallstones, the gallbladder epithelium aids in the establishment/maintenance of chronic carriage. In this work, we present evidence of the role of the gallbladder epithelium in chronic carriage by a mechanism involving invasion, intracellular persistence andbiofilm formation. Salmonella was able to adhere to and invade polarized gallbladder epithelial cells apically in the absence and presence of bile in a SPI-1 dependent manner.
Intracellular replication of Salmonella was also evident at 12 and 24 hours post-invasion. A flow-through system revealed that Salmonella is able to adhere to and form extensive bacterial foci on gallbladder epithelial cell as soon as 12 hours post-inoculation. In vivo experiments using a chronic mouse model of typhoid carriage showed invasion and damage of the gallbladder epithelium and lamina propria up to 2 months after Salmonella infection with an abundant presence of macrophages, a relative absence of neutrophils, and extrusion of infected epithelial cells. Additionally, micro-colonies of Salmonella cells were evident on the surface of the mouse gallbladder epithelia up to 21 days post-infection. These data reveal a second potential mechanism, intracellular persistence and/or bacterial aggregation in/on the gallbladder epithelium with luminal cell extrusion, for Salmonella maintenance in the gallbladder.
PMID: 23732169 [PubMed – as supp
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