Salmonella Typhimurium discreet-invasion of the murine gut absorptive epithelium.
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AuthorsFattinger, Stefan A
Di Martino, Maria Letizia
Samperio Ventayol, Pilar
Müller-Hauser, Anna A
Nguyen, Bidong D
Sellin, Mikael E
MetadataShow full item record
AbstractSalmonella enterica serovar Typhimurium (S.Tm) infections of cultured cell lines have given rise to the ruffle model for epithelial cell invasion. According to this model, the Type-Three-Secretion-System-1 (TTSS-1) effectors SopB, SopE and SopE2 drive an explosive actin nucleation cascade, resulting in large lamellipodia- and filopodia-containing ruffles and cooperative S.Tm uptake. However, cell line experiments poorly recapitulate many of the cell and tissue features encountered in the host's gut mucosa. Here, we employed bacterial genetics and multiple imaging modalities to compare S.Tm invasion of cultured epithelial cell lines and the gut absorptive epithelium in vivo in mice. In contrast to the prevailing ruffle-model, we find that absorptive epithelial cell entry in the mouse gut occurs through "discreet-invasion". This distinct entry mode requires the conserved TTSS-1 effector SipA, involves modest elongation of local microvilli in the absence of expansive ruffles, and does not favor cooperative invasion. Discreet-invasion preferentially targets apicolateral hot spots at cell-cell junctions and shows strong dependence on local cell neighborhood. This proof-of-principle evidence challenges the current model for how S.Tm can enter gut absorptive epithelial cells in their intact in vivo context.
CitationPLoS Pathog. 2020 May 4;16(5):e1008503. doi: 10.1371/journal.ppat.1008503.
AffiliationHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
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- Barcoded Consortium Infections Resolve Cell Type-Dependent Salmonella enterica Serovar Typhimurium Entry Mechanisms.
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- Authors: Hapfelmeier S, Ehrbar K, Stecher B, Barthel M, Kremer M, Hardt WD
- Issue date: 2004 Feb
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- Authors: Perrett CA, Jepson MA
- Issue date: 2009 Mar
- Salmonella enterica Serovar Typhimurium Exploits Cycling through Epithelial Cells To Colonize Human and Murine Enteroids.
- Authors: Geiser P, Di Martino ML, Samperio Ventayol P, Eriksson J, Sima E, Al-Saffar AK, Ahl D, Phillipson M, Webb DL, Sundbom M, Hellström PM, Sellin ME
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- Authors: Giacomodonato MN, Uzzau S, Bacciu D, Caccuri R, Sarnacki SH, Rubino S, Cerquetti MC
- Issue date: 2007 Apr