Ethanolamine Signaling Promotes Salmonella Niche Recognition and Adaptation during Infection

Anderson, Christopher J.; Clark, David E.; Adli, Mazhar; Kendall, Melissa M.

doi:10.1371/journal.ppat.1005278

Cited by 76 publications

(111 citation statements)

References 66 publications

Supporting

Mentioning

105

Contrasting

Order By: Relevance

“…Moreover, S . Typhimurium uses ethanolamine for signaling to recognize and adapt to different niches within the host, leading to successful intestinal infection and intramacrophage survival [72]. We speculate that Salmonella could be using the ethanolamine from cell membranes abundantly present due to cell death and inflammation damage within tumor tissue.…”

Section: Discussionmentioning

confidence: 99%

Solid tumors provide niche-specific conditions that lead to preferential growth of Salmonella

et al. 2016

View full text Add to dashboard Cite

Therapeutic attenuated strains of Salmonella Typhimurium target and eradicate tumors in mouse models. However, the mechanism of S. Typhimurium for tumor targeting is still poorly understood. We performed a high-throughput screening of single-gene deletion mutants of S. Typhimurium in an orthotopic, syngeneic murine mammary model of breast cancer. The mutants under selection in this system were classified into functional categories to identify bacterial processes involved in Salmonella accumulation within tumors. Niche-specific genes involved in preferential tumor colonization were identified and exemplars were confirmed by competitive infection assays. Our results show that the chemotaxis gene cheY and the motility genes motAB confer an advantage for colonization of Salmonella within orthotopic syngeneic breast tumors. In addition, eutC, a gene belonging to the ethanolamine metabolic pathway, also confers an advantage for Salmonella within tumors, perhaps by exploiting either ethanolamine or an alternative nutrient in the inflamed tumor environment.

show abstract

Section: Discussionmentioning

confidence: 99%

Solid tumors provide niche-specific conditions that lead to preferential growth of Salmonella

et al. 2016

View full text Add to dashboard Cite

show abstract

“…RNA purification and quantification of RNA transcription were performed as described previously (43). RNA was extracted from three biological replicate cultures of each strain/ condition using a RiboPure Bacteria RNA isolation kit (Ambion).…”

Section: Methodsmentioning

confidence: 99%

The Type Three Secretion System 2-Encoded Regulator EtrB Modulates Enterohemorrhagic Escherichia coli Virulence Gene Expression

et al. 2016

Self Cite

View full text Add to dashboard Cite

bEnterohemorrhagic Escherichia coli O157:H7 (EHEC) is a foodborne pathogen that causes bloody diarrhea and hemolytic uremic syndrome throughout the world. A defining feature of EHEC pathogenesis is the formation of attaching and effacing (AE) lesions on colonic epithelial cells. Most of the genes that code for AE lesion formation, including a type three secretion system (T3SS) and effectors, are carried within a chromosomal pathogenicity island called the locus of enterocyte effacement (LEE). In this study, we report that a putative regulator, which is encoded in the cryptic E. coli type three secretion system 2 (ETT2) locus and herein renamed EtrB, plays an important role in EHEC pathogenesis. The etrB gene is expressed as a monocistronic transcript, and EtrB autoregulates expression. We provide evidence that EtrB directly interacts with the ler regulatory region to activate LEE expression and promote AE lesion formation. Additionally, we mapped the EtrB regulatory circuit in EHEC to determine a global role for EtrB. EtrB is regulated by the transcription factor QseA, suggesting that these proteins comprise a regulatory circuit important for EHEC colonization of the gastrointestinal tract.

show abstract

“…Several EHEC virulence genes are induced by EA via the expression of the EutR factor, an EA receptor. Genes induced by EA via EutR include genes encoding fimbrial adhesins, flagella, Shiga toxin, and the LEE (95,121).…”

Section: The Role Of Other Metabolites In Bacterial Pathogenesismentioning

confidence: 99%

Bacterial Chat: Intestinal Metabolites and Signals in Host-Microbiota-Pathogen Interactions

2017

View full text Add to dashboard Cite

Intestinal bacteria employ microbial metabolites from the microbiota and chemical signaling during cell-to-cell communication to regulate several cellular functions. Pathogenic bacteria are extremely efficient in orchestrating their response to these signals through complex signaling transduction systems. Precise coordination and interpretation of these multiple chemical cues is important within the gastrointestinal (GI) tract. Enteric foodborne pathogens, such as enterohemorrhagic Escherichia coli (EHEC) and Salmonella enterica serovar Typhimurium, or the surrogate murine infection model for EHEC, Citrobacter rodentium, are all examples of microorganisms that modulate the expression of their virulence repertoire in response to signals from the microbiota or the host, such as autoinducer-3 (AI-3), epinephrine (Epi), and norepinephrine (NE). The QseBC and QseEF two-component systems, shared by these pathogens, are involved in sensing these signals. We review how these signaling systems sense and relay these signals to drive bacterial gene expression; specifically, to modulate virulence. We also review how bacteria chat via chemical signals integrated with metabolite recognition and utilization to promote successful associations among enteric pathogens, the microbiota, and the host. KEYWORDS chemical signaling, Enterobacteriaceae, Escherichia, Salmonella, intestinal metabolites COMMENSALS AND PATHOGENS IN THE GUTT he large and diverse bacterial community in the human gut also has important functions in the physiology of the intestine. The intestinal mucosa forms a physical barrier that keeps the microbiota on the luminal side. The mucus layer is composed of mucin, glycoproteins, trefoil peptides, and surfactant phospholipids (Fig. 1). Altogether, they constitute a nutrient-rich mucus layer, which has an important role as a protective barrier against microorganisms (1). The biogeography of the gastrointestinal (GI) tract is diverse in its composition and density and its distinct chemical and physical features (2). The density and composition of bacterial communities change according to their location in the gut. Throughout the GI tract, there is significant variation in the physicochemical conditions and substrate availability that impact bacterial growth, differentially promoting or hampering the colonization of certain niches by various species. In the proximal colon, the high concentration of sugar substrates in the mucus allows the expansion of the saccharolytic members of the microbiota (Table 1). Inversely, the lower availability of sugar substrates in the distal colon triggers proteolysis, which decreases the bacterial growth rate and the diversity of the microbiota (1, 3). The resident microbiota, together with all chemical and physical features of the intestine, contribute to shape the metabolic landscape within the gut, producing a multitude of characterized and as-yet-unknown intestinal metabolites. Moreover, the microbial composition of the human GI tract varies with age, diet, host genetics, a...

show abstract

Ethanolamine Signaling Promotes Salmonella Niche Recognition and Adaptation during Infection

Cited by 76 publications

References 66 publications

Solid tumors provide niche-specific conditions that lead to preferential growth of Salmonella

Solid tumors provide niche-specific conditions that lead to preferential growth of Salmonella

The Type Three Secretion System 2-Encoded Regulator EtrB Modulates Enterohemorrhagic Escherichia coli Virulence Gene Expression

Bacterial Chat: Intestinal Metabolites and Signals in Host-Microbiota-Pathogen Interactions

Contact Info

Product

Resources

About