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A role for the Salmonella Type III Secretion System 1 in bacterial adaptation to the cytosol of epithelial cells

Summary Salmonella enterica serovar Typhimurium is a facultative intracellular pathogen that invades the intestinal epithelium. Following invasion of epithelial cells, Salmonella survives and replicates within two distinct intracellular niches. While all of the bacteria are initially taken up into a...

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Bibliographic Details
Published in:Molecular microbiology 2019-10, Vol.112 (4), p.1270-1283
Main Authors: Chong, Audrey, Starr, Tregei, Finn, Ciaran E., Steele‐Mortimer, Olivia
Format: Article
Language:English
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Summary:Summary Salmonella enterica serovar Typhimurium is a facultative intracellular pathogen that invades the intestinal epithelium. Following invasion of epithelial cells, Salmonella survives and replicates within two distinct intracellular niches. While all of the bacteria are initially taken up into a membrane bound vacuole, the Salmonella‐containing vacuole or SCV, a significant proportion of them promptly escape into the cytosol. Cytosolic Salmonella replicates more rapidly compared to the vacuolar population, although the reasons for this are not well understood. SipA, a multi‐function effector protein, has been shown to affect intracellular replication and is secreted by cytosolic Salmonella via the invasion‐associated Type III Secretion System 1 (T3SS1). Here, we have used a multipronged microscopy approach to show that SipA does not affect bacterial replication rates per se, but rather mediates intra‐cytosolic survival and/or initiation of replication following bacterial egress from the SCV. Altogether, our findings reveal an important role for SipA in the early survival of cytosolic Salmonella. The bacterial pathogen Salmonella Typhimurium invades intestinal epithelial cells. Following invasion, the bacteria can either replicate within a membrane bound vacuole or escape into the cytosol. We show here that SipA, a secreted bacterial protein, facilitates the early survival and/or initiation of replication of cytosolic Salmonella.
ISSN:0950-382X
1365-2958
DOI:10.1111/mmi.14361