Quorum sensing in Escherichia coli and Salmonella

Walters, Matthew S.; Sperandio, Vanessa

doi:10.1016/j.ijmm.2006.01.041

Cited by 194 publications

(147 citation statements)

References 49 publications

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“…Although a number of interesting molecules such as the catecholamine epinephrine (Kobashi et al, 1987), known to affect virulence gene expression in intestinal pathogens (Walters & Sperandio, 2006), and various phenolic antibiotics (Kim et al, 1992) have been shown in vitro to be modified by ASST enzymes, we have shown that loss of assT confers no phenotype during acute Salmonella infection in mice. Mutations in assT do confer a defect in long-term infection of mice (Lawley et al, 2006).…”

Section: Discussionmentioning

confidence: 70%

DsbL and DsbI contribute to periplasmic disulfide bond formation in Salmonella enterica serovar Typhimurium

2009

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Disulfide bond formation in periplasmic proteins is catalysed by the DsbA/DsbB system in most Gram-negative bacteria. Salmonella enterica serovar Typhimurium also encodes a paralogous pair of proteins to DsbA and DsbB, DsbL and DsbI, respectively, downstream of a periplasmic arylsulfate sulfotransferase (ASST). We show that DsbL and DsbI function as a redox pair contributing to periplasmic disulfide bond formation and, as such, affect transcription of the Salmonella pathogenicity island 1 (SPI1) type three secretion system genes and activation of the RcsCDB system, as well as ASST activity. In contrast to DsbA/DsbB, however, the DsbL/DsbI system cannot catalyse the disulfide bond formation required for flagellar assembly. Phylogenic analysis suggests that the assT dsbL dsbI genes are ancestral in the Enterobacteriaceae, but have been lost in many lineages. Deletion of assT confers no virulence defect during acute Salmonella infection of mice.

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Section: Discussionmentioning

confidence: 70%

DsbL and DsbI contribute to periplasmic disulfide bond formation in Salmonella enterica serovar Typhimurium

2009

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“…QseG is an outer-membrane protein and it is also required for the translocation of type III secretion system effectors into host cells (Reading et al, 2009). Besides these two-component systems, two LysRtype regulators, QseA and QseD, are also required for the control of LEE expression, revealing that a complex regulatory cascade links quorum sensing and virulence gene expression in E. coli (Sperandio et al, 2002a;Walters & Sperandio, 2006).…”

Section: Quorum Sensing In Escherichia Coli Virulencementioning

confidence: 99%

Quorum sensing in bacterial virulence

et al. 2010

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Bacteria communicate through the production of diffusible signal molecules termed autoinducers. The molecules are produced at basal levels and accumulate during growth. Once a critical concentration has been reached, autoinducers can activate or repress a number of target genes. Because the control of gene expression by autoinducers is cell-density-dependent, this phenomenon has been called quorum sensing. Quorum sensing controls virulence gene expression in numerous micro-organisms. In some cases, this phenomenon has proven relevant for bacterial virulence in vivo. In this article, we provide a few examples to illustrate how quorum sensing can act to control bacterial virulence in a multitude of ways. Several classes of autoinducers have been described to date and we present examples of how each of the major types of autoinducer can be involved in bacterial virulence. As quorum sensing controls virulence, it has been considered an attractive target for the development of new therapeutic strategies. We discuss some of the new strategies to combat bacterial virulence based on the inhibition of bacterial quorum sensing systems.

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“…On the other hand, the luxS gene is responsible for Salmonella AI-2 synthesis (Table 2). Some reports have also described the ability of Salmonella to sense and respond to neurotransmitters and hormones produced by the host, such as epinephrine and norepinephrine (Walters & Sperandio, 2006;.…”

Section: D Gel Electrophoresis Analyses By Vanmentioning

confidence: 99%

Salmonella spp. survival strategies within the host gastrointestinal tract

et al. 2011

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Human salmonellosis infections are usually acquired via the food chain as a result of the ability of Salmonella serovars to colonize and persist within the gastrointestinal tract of their hosts. In addition, after food ingestion and in order to cause foodborne disease in humans, Salmonella must be able to resist several deleterious stress conditions which are part of the host defence against infections. This review gives an overview of the main defensive mechanisms involved in the Salmonella response to the extreme acid conditions of the stomach, and the elevated concentrations of bile salts, osmolytes and commensal bacterial metabolites, and the low oxygen tension conditions of the mammalian and avian gastrointestinal tracts.

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Quorum sensing in Escherichia coli and Salmonella

Cited by 194 publications

References 49 publications

DsbL and DsbI contribute to periplasmic disulfide bond formation in Salmonella enterica serovar Typhimurium

DsbL and DsbI contribute to periplasmic disulfide bond formation in Salmonella enterica serovar Typhimurium

Quorum sensing in bacterial virulence

Salmonella spp. survival strategies within the host gastrointestinal tract

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