Two newly identified SipA domains (F1, F2) steer effector protein localization and contribute to <i>Salmonella</i> host cell manipulation

Schlumberger, Markus C.; Käppeli, Rina; Wetter, Michael; Müller, Andreas J.; Misselwitz, Benjamin; Dilling, Sabrina; Kremer, Marcus; Hardt, Wolf‐Dietrich

doi:10.1111/j.1365-2958.2007.05823.x

Cited by 40 publications

(52 citation statements)

References 51 publications

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“…Nine images per well (approximately 6,000 cells) were taken in the GFP and DAPI channels, using a CellWorx automated microscope (API). Image processing was done using CellProfiler (7) and customized Matlab scripts, as described previously (26). Any cell harboring GFP-expressing bacteria was considered "infected.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, we performed a host cell invasion assay to further analyze the virulence of the serovar Enteritidis and Typhimurium strains. We recently developed a high-throughput format for quantitative analysis of Salmonella invasion into HeLa cells (26). In this assay, cells are infected with serovar Enteritidis and Typhimurium strains harboring a plasmid expressing GFP under the control of a SPI-2 promoter (pM975) (see Materials and Methods), and invading bacteria are detected by automated microscopy by virtue of their GFP expression.…”

Section: Downloaded Frommentioning

confidence: 99%

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Accelerated Type III Secretion System 2-Dependent Enteropathogenesis by a Salmonella enterica Serovar Enteritidis PT4/6 Strain

et al. 2009

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Salmonella enterica subsp. I serovars Typhimurium and Enteritidis are major causes of enteric disease. The pathomechanism of enteric infection by serovar Typhimurium has been studied in detail. Serovar Typhimurium employs two pathways in parallel for triggering disease, i.e., the "classical" pathway, triggered by type III secretion system 1 (TTSS-1), and the "alternative" pathway, mediated by TTSS-2. It had remained unclear whether these two pathways would also explain the enteropathogenesis of strains from other serovars. We chose the isolate P125109 of the epidemic serovar Enteritidis PT4/6, generated isogenic mutants, and studied their virulence. Using in vitro and in vivo infection experiments, a dendritic cell depletion strategy, and MyD88 ؊/؊ knockout mice, we found that P125109 employs both the "classical" and "alternative" pathways for triggering mucosal inflammation. The "classical" pathway was phenotypically similar in serovar Typhimurium strain SL1344 and in P125109. However, the kinetics of the "alternative" pathway differed significantly. Via TTSS-2, P125109 colonized the gut tissue more efficiently and triggered mucosal inflammation approximately 1 day faster than SL1344 did. In conclusion, our data demonstrate that different Salmonella spp. can differ in their capacity to trigger mucosal inflammation via the "alternative" pathway in vivo.

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Section: Methodsmentioning

confidence: 99%

Section: Downloaded Frommentioning

confidence: 99%

Accelerated Type III Secretion System 2-Dependent Enteropathogenesis by a Salmonella enterica Serovar Enteritidis PT4/6 Strain

et al. 2009

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“…[8][9][10][11] Bacterial genes (SPI-1 and SPI-2 encoded factors) were also shown to be critical during this infection stage. [12][13][14][15] Besides the fact that this model of infection causes a systemic disease with typhoid-like symptoms in the majority of inbred strains, the Salmonella Typhimurium oral infection model remains relevant to study initial steps affecting the colonization of the host.…”

Section: Introductionmentioning

confidence: 99%

Impact of Usp18 and IFN signaling in Salmonella-induced typhlitis

et al. 2011

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In humans, Salmonella infection causes two major clinical diseases, typhoid fever and a self-limiting gastro-enteritidis. Salmonella transmission occurs by the fecal-oral route and the interactions between the bacteria and the digestive tract epithelium are central to the outcome of the infection. Using a mouse model of typhoid fever, we previously identified a mutation in USP18 affecting type I interferon (IFN) signaling resulting in increased susceptibility to systemic Salmonella infection. In this study, we demonstrate the effects of this mutation during the early response to Salmonella using a model of typhlitis. Mutant Usp18 mice showed a minimal inflammatory response early after Salmonella Typhimurium infection that was associated with low pathologic scores and low IFN-g production. This resulted in an increased interaction of Salmonella with the cecal epithelium and earlier systemic dissemination of the bacteria. The global transcriptional signature in the cecum of mouse during Salmonella infection showed normal expression of tissue specific genes and upregulation of type I IFN pathway in mutant mice. In control mice, there was a significant over-representation of genes involved in cellular recruitment and antibacterial activity paralleling the histopathological features. These results show the impact of USP18 in the development of Salmonella-induced typhlitis.

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“…1B), which are also the sites of S. Typhimurium invasion. S. Typhimurium mutants with an intact T1 apparatus, but lacking SopE, SopE2, SipA, and SopB, do not trigger actin rearrangements or membrane ruffling and are impaired in cellular invasion (48,59,70). These types of S. Typhimurium mutants facilitated the discovery of the binding phenotype of T1 (42).…”

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Salmonella entericaSerovar Typhimurium Binds to HeLa Cells via Fim-Mediated Reversible Adhesion and Irreversible Type Three Secretion System 1-Mediated Docking

et al. 2011

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Two newly identified SipA domains (F1, F2) steer effector protein localization and contribute to Salmonella host cell manipulation

Abstract: Summary Salmonella

Cited by 40 publications

References 51 publications

Accelerated Type III Secretion System 2-Dependent Enteropathogenesis by a Salmonella enterica Serovar Enteritidis PT4/6 Strain

Accelerated Type III Secretion System 2-Dependent Enteropathogenesis by a Salmonella enterica Serovar Enteritidis PT4/6 Strain

Impact of Usp18 and IFN signaling in Salmonella-induced typhlitis

Salmonella entericaSerovar Typhimurium Binds to HeLa Cells via Fim-Mediated Reversible Adhesion and Irreversible Type Three Secretion System 1-Mediated Docking

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