The Salmonella enterica serotype Typhi regulator TviA reduces interleukin-8 production in intestinal epithelial cells by repressing flagellin secretion

Winter, Sebastian; Raffatellu, Manuela; Wilson, Ronald P.; Rüssmann, Holger; Bäumler, Andreas J.

doi:10.1111/j.1462-5822.2007.01037.x

Cited by 73 publications

(102 citation statements)

References 56 publications

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“…However, higher levels of IL-6 mRNA in the caecal tonsils of SG-infected birds suggested that the pro-inflammatory immune response elicited in lymphoid tissue has a different pattern from that observed in vitro with SG-infected epithelial cells and may involve different cell types. A similar picture was observed in epithelial cell lines infected with S. enterica serovar Typhi, which triggered antagonistic patterns of IL-8 expression in the early stages of infection (Winter et al, 2008;Fiorentino et al, 2013).…”

Section: Article In Presssupporting

confidence: 52%

Experimental infection of chickens by a flagellated motile strain of Salmonella enterica serovar Gallinarum biovar Gallinarum

Lopes

Neto

Batista

et al. 2016

The Veterinary Journal

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Section: Article In Presssupporting

confidence: 52%

Experimental infection of chickens by a flagellated motile strain of Salmonella enterica serovar Gallinarum biovar Gallinarum

Lopes

Neto

Batista

et al. 2016

The Veterinary Journal

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“…It has also been shown that non-flagellar mutants of S. Enteritidis are strongly attenuated in their ability to invade cultured epithelial cells (Dibb-Fuller et al, 1999;van Asten et al, 2000), further suggesting that lower virulence of low invasiveness isolates is at least in part associated with their impaired motility (Table 4). It has been proposed that in S. Typhi, a host-adapted serotype, repression of flagellin may facilitate evasion from TLR5-mediated innate responses of host mucosal epithelium, thereby enhancing systemic bacterial dissemination from the intestine (Winter et al, 2008(Winter et al, , 2010. Repression of flagellin was also shown to enable increased dissemination of S. Typhimurium to the spleen in a chicken model (Winter et al, 2010).…”

Section: Discussionmentioning

confidence: 91%

Cell invasion of poultry-associated Salmonella enterica serovar Enteritidis isolates is associated with pathogenicity, motility and proteins secreted by the type III secretion system

et al. 2011

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Salmonella enterica serovar Enteritidis (S. Enteritidis) is a major cause of food-borne gastroenteritis in humans worldwide. Poultry and poultry products are considered the major vehicles of transmission to humans. Using cell invasiveness as a surrogate marker for pathogenicity, we tested the invasiveness of 53 poultry-associated isolates of S. Enteritidis in a well-differentiated intestinal epithelial cell model (Caco-2). The method allowed classification of the isolates into low (n57), medium (n518) and high (n530) invasiveness categories. Cell invasiveness of the isolates did not correlate with the presence of the virulence-associated gene spvB or the ability of the isolates to form biofilms. Testing of representative isolates with high and low invasiveness in a mouse model revealed that the former were more invasive in vivo and caused more and earlier mortalities, whereas the latter were significantly less invasive in vivo, causing few or no mortalities. Further characterization of representative isolates with low and high invasiveness showed that most of the isolates with low invasiveness had impaired motility and impaired secretion of either flagella-associated proteins (FlgK, FljB and FlgL) or type III secretion system (TTSS)-secreted proteins (SipA and SipD) encoded on Salmonella pathogenicity island-1. In addition, isolates with low invasiveness had impaired ability to invade and/or survive within chicken macrophages. These data suggest that not all isolates of S. Enteritidis recovered from poultry may be equally pathogenic, and that the pathogenicity of S. Enteritidis isolates is associated, in part, with both motility and secretion of TTSS effector proteins. INTRODUCTIONSalmonella enterica serovar Enteritidis (S. Enteritidis) is the leading cause of food-borne salmonellosis (WHO, 2008). S. Enteritidis-induced salmonellosis in humans is characterized by diarrhoea, fever, headache, abdominal pain, nausea and vomiting (CDC, 2007). S. Enteritidis is also increasingly reported from cases of invasive and extra-intestinal infections such as septicaemia, arthritis, endocarditis, meningitis and urinary tract infections (Ghosh & Vogt, 2006; Gordon et al., 2008;Katsenos et al., 2008; Kobayashi et al., 2009;Morpeth et al., 2009;Mutlu et al., 2009;Tena et al., 2007). Between 1990 and 2001, the US state and territorial health departments reported 677 S. Enteritidis outbreaks, which accounted for 23 366 illnesses, 1988 hospitalizations and 33 deaths (CDC, 2003). In 2006, countries within the European Union reported 1729 outbreaks caused by S. Enteritidis leading to 13 853 illnesses, 2714 hospitalizations and 14 deaths (EFSA, 2007). The Health Protection Agency of the UK reported 4194 cases of foodborne S. Enteritidis infection in (HPA, 2008. Poultry is considered the single largest reservoir of S. Enteritidis and most risk attribution studies have identified poultry and poultry products as the major source of human infection. S. Enteritidis is passed to humans mainly via handling and consumption of contaminated po...

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“…by down-regulating flagellin expression (Winter et al, 2008) or modifying LPS (Guo et al, 1997;Matsuura et al, 2012) of the commensal microbiota that often lack the capability to utilize these compounds (Thiennimitr et al, 2012). S. Typhimurium appears to be an ideal choice as a model organism for the establishment of a novel host-pathogen transcriptomic approach.…”

Section: Salmonella As a Model Organism For Host-pathogen Interactionmentioning

confidence: 99%

Dual RNA-seq of pathogen and host

2012

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SummaryThe infection of a eukaryotic host cell by a bacterial pathogen is one of the most intimate examples of cross-kingdom interactions in biology. Infection processes are highly relevant from both a basic research as well as a clinical point of view. Sophisticated mechanisms have evolved in the pathogen to manipulate the host response and vice versa host cells have developed a wide range of anti-microbial defense strategies to combat bacterial invasion and clear infections.However, it is this diversity and complexity that makes infection research so challenging to technically address as common approaches have either been optimized for bacterial or eukaryotic organisms. Instead, methods are required that are able to deal with the often dramatic discrepancy between host and pathogen with respect to various cellular properties and processes. One class of cellular macromolecules that exemplify this host-pathogen heterogeneity is given by their transcriptomes: Bacterial transcripts differ from their eukaryotic counterparts in many aspects that involve both quantitative and qualitative traits. The entity of RNA transcripts present in a cell is of paramount interest as it reflects the cell's physiological state under the given condition. Genome-wide transcriptomic techniques such as RNA-seq have therefore been used for single-organism analyses for several years, but their applicability has been limited for infection studies.The present work describes the establishment of a novel transcriptomic approach for infection biology which we have termed "Dual RNA-seq". Using this technology, it was intended to shed light particularly on the contribution of non-protein-encoding transcripts to virulence, as these classes have mostly evaded previous infection studies due to the lack of suitable methods. The performance of Dual RNA-seq was evaluated in an in vitro infection model based on the important facultative intracellular pathogen Salmonella enterica serovar Typhimurium and different human cell lines. Dual RNA-seq was found to be capable of capturing all major bacterial and human transcript classes and proved reproducible. During the course of these experiments, a previously largely uncharacterized bacterial small non-coding RNA (sRNA), referred to as STnc440, was identified as one of the most strongly induced genes in intracellular Salmonella.Interestingly, while inhibition of STnc440 expression has been previously shown to cause a virulence defect in different animal models of Salmonellosis, the underlying molecular mechanisms have remained obscure. Here, classical genetics, transcriptomics and biochemical assays proposed a complex model of Salmonella gene expression control that is orchestrated by this sRNA. In particular, STnc440 was found to be involved in the regulation of multiple bacterial target mRNAs by direct base pair interaction with consequences for Salmonella virulence and

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The Salmonella enterica serotype Typhi regulator TviA reduces interleukin-8 production in intestinal epithelial cells by repressing flagellin secretion

Cited by 73 publications

References 56 publications

Experimental infection of chickens by a flagellated motile strain of Salmonella enterica serovar Gallinarum biovar Gallinarum

Experimental infection of chickens by a flagellated motile strain of Salmonella enterica serovar Gallinarum biovar Gallinarum

Cell invasion of poultry-associated Salmonella enterica serovar Enteritidis isolates is associated with pathogenicity, motility and proteins secreted by the type III secretion system

Dual RNA-seq of pathogen and host

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