Salmonella enterica Serovar Typhi Conceals the Invasion-Associated Type Three Secretion System from the Innate Immune System by Gene Regulation
Sebastian E. Winter,Maria G. Winter,Maria G. Winter,Victor Poon,A. Marijke Keestra,Torsten Sterzenbach,Franziska Faber,Luciana F. Costa,Fabiane Cassou,Érica Azevedo Costa,Geraldo Eleno Silveira Alves,Tatiane A. Paixão,Renato L. Santos,Andreas J. Bäumler +13 more
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TLDR
It is shown that Salmonella enterica serovar Typhi, the causative agent of typhoid fever, tightly regulates expression of the invasion-associated type III secretion system (T3SS-1) and thus fails to activate these innate immune signaling pathways.Abstract:
Delivery of microbial products into the mammalian cell cytosol by bacterial secretion systems is a strong stimulus for triggering pro-inflammatory host responses. Here we show that Salmonella enterica serovar Typhi (S. Typhi), the causative agent of typhoid fever, tightly regulates expression of the invasion-associated type III secretion system (T3SS-1) and thus fails to activate these innate immune signaling pathways. The S. Typhi regulatory protein TviA rapidly repressed T3SS-1 expression, thereby preventing RAC1-dependent, RIP2-dependent activation of NF-κB in epithelial cells. Heterologous expression of TviA in S. enterica serovar Typhimurium (S. Typhimurium) suppressed T3SS-1-dependent inflammatory responses generated early after infection in animal models of gastroenteritis. These results suggest that S. Typhi reduces intestinal inflammation by limiting the induction of pathogen-induced processes through regulation of virulence gene expression.read more
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Now you see me, now you don't: the interaction of Salmonella with innate immune receptors
TL;DR: This Review compares and contrast the interactions of S. Typhi and NTS serovars with host innate immune receptors and discusses why the disease manifestations associated with S. typhi infection differ considerably from those associated with the closely related NTSSerovars.
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An Oxidative Central Metabolism Enables Salmonella to Utilize Microbiota-Derived Succinate.
Luisella Spiga,Maria G. Winter,Tatiane Furtado de Carvalho,Wenhan Zhu,Elizabeth R. Hughes,Caroline C. Gillis,Cassie L. Behrendt,Jiwoong Kim,Daniela Chessa,Helene Andrews-Polymenis,Daniel P. Beiting,Renato L. Santos,Lora V. Hooper,Sebastian E. Winter +13 more
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Interactions of Salmonella with animals and plants
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Non-typhoidal Salmonella Typhimurium ST313 isolates that cause bacteremia in humans stimulate less inflammasome activation than ST19 isolates associated with gastroenteritis.
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Lutgart Overbergh,Annapaula Giulietti,Dirk Valckx,Brigitte Decallonne,Roger Bouillon,Chantal Mathieu +5 more
TL;DR: The development of real-time RT-PCR has resulted in an exponential increase in its use over the last couple of years, and the method has undoubtedly become the standard for quantifying cytokine patterns, clarifying many functional properties of immune cells and their associated diseases.
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hilA is a novel ompR/toxR family member that activates the expression of Salmonella typhimurium invasion genes
TL;DR: By using a set of lacZY transcriptional fusions to S. typhimurium invasion genes, it is found that hilA activates the expression of invasion genes located on the ‘pathogenicity island’, consistent with the hypothesis that hILA plays a key role in the regulation of Salmonella invasion during infection.
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The Salmonella Pathogenicity Island (SPI)-2 and SPI-1 Type III Secretion Systems Allow Salmonella Serovar typhimurium to Trigger Colitis via MyD88-Dependent and MyD88-Independent Mechanisms
Siegfried Hapfelmeier,Bärbel Stecher,Manja Barthel,Marcus Kremer,Andreas Müller,Mathias Heikenwalder,Thomas Stallmach,Michael Hensel,Klaus Pfeffer,Shizuo Akira,Wolf-Dietrich Hardt +10 more
TL;DR: S. typhimurium can use two independent mechanisms to elicit colitis in vivo: SPI-1-dependent and MyD 88-independent signaling to epithelial cells and SPI-2-dependent intracellular proliferation in the lamina propria triggering MyD88-dependent innate immune responses.