Nutrient and chemical sensing by intestinal pathogens

Hernandez-Doria, Juan D.; Sperandio, Vanessa

doi:10.1016/j.micinf.2013.06.013

Cited by 17 publications

(11 citation statements)

References 70 publications

(108 reference statements)

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“…Diet influences nutrient availability in the gut and changes the composition of the intestinal microbiota. Pathogenic bacteria generally compete directly against commensals for nutrients and colonization sites within the intestine (18,19).…”

Section: From Food Sources To Microbial Metabolismmentioning

confidence: 99%

“…Commensal E. coli colonizes the human GI tract within a few hours after birth, initiating a mutually beneficial relationship (14). Pathogenic E. coli employs complex virulence mechanisms that are activated by chemical signaling and nutrients, both essential for intestinal colonization and evasion of host defenses (19,25).…”

Section: Bacterial Metabolite Sensingmentioning

confidence: 99%

“…The chemical and nutrient signaling in these bacteria is mediated by two-component systems (TCS), such as QseBC and QseEF, that sense these differences and initiate a complex signaling cascade that drives the virulence program in these pathogens ( Fig. 2) (15,19). The bacterial enteric community is a complex system and suffers constant exposure to threats, such as potential pathogens.…”

Section: Bacterial Metabolite Sensingmentioning

confidence: 99%

“…EHEC harbors a pathogenicity island named the locus of enterocyte effacement (LEE), which encodes a microscopic "needle," a type III secretion system (T3SS), that injects many different effector proteins into the host cell ( Fig. 1) (19,28,(31)(32)(33)(34)(35). In addition to the T3SS, the LEE also contains genes that encode an adhesin (intimin) (36) and its own receptor, the translocated intimin receptor (Tir) (37,38), which is translocated into the epithelial cell (33)(34)(35).…”

Section: Bacterial Pathogenesis Controlled By Intestinal Chemical Senmentioning

confidence: 99%

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

2017

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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...

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Section: From Food Sources To Microbial Metabolismmentioning

confidence: 99%

Section: Bacterial Metabolite Sensingmentioning

confidence: 99%

Section: Bacterial Metabolite Sensingmentioning

confidence: 99%

Section: Bacterial Pathogenesis Controlled By Intestinal Chemical Senmentioning

confidence: 99%

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

2017

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“…Like other enteric pathogens, EHEC uses many hostand microbiota-derived chemicals to regulate virulence gene expression when in the host (107). To date, only a few of these have been described.…”

Section: Role Of the Host In Modulating Ehec Virulencementioning

confidence: 99%

Animal Models of EnterohemorrhagicEscherichia coliInfection

Ritchie

2014

Microbiol Spectr

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The first major outbreaks caused by enterohemorrhagic Escherichia coli (EHEC) raised public and medical awareness of the risks associated with acquiring this potentially deadly infection. The widespread presence of these organisms in the environment, the severity of the clinical sequelae, and the lack of treatment options and effective preventive measures demand that we obtain a better understanding of how this group of organisms cause disease. Animal models allow study of the processes and factors that contribute to disease and, as such, form a valuable tool in the repertoire of infectious disease researchers. Yet despite more than 30 years of research, it seems that no single model host reproduces the full spectrum of clinical disease induced by EHEC in humans. In the first part of this review, a synopsis of what is known about EHEC infections is garnered from human outbreaks and biopsy specimens. The main features and limitations of EHEC infection models that are based on the three most commonly used species (pigs, rabbits, and mice) are described within a historical context. Recent advances are highlighted, and a brief overview of models based on other species is given. Finally, the impact of the host on moderating EHEC infection is considered in light of growing evidence for the need to consider the biology and virulence strategies of EHEC in the context of its niche within the intestine.

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Responses in ileal and cecal bacteria to low and high amylose/amylopectin ratio diets in growing pigs

Luo

Yang

Wright

et al. 2015

Appl Microbiol Biotechnol

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Dietary starch that escapes digestion in the small intestine may serve as a carbon source for bacterial fermentation in the distal intestine. This study aimed to compare the bacterial community in the ileal and cecal digesta of growing pigs fed diets with low (0.14, LR pigs) and high (0.43, HR pigs) amylose/amylopectin ratio. Pyrosequencing based on MiSeq 2000 platform showed that in ileum digesta, Bacteroidetes of LR pigs was markedly higher than that in HR pigs (P < 0.05). Megasphaera and Prevotella were the two most predominant genera in LR pigs, and Prevotella was significantly higher in LR pigs than in HR pigs (P < 0.05). Prevotella was predominant in cecal samples from both LR and HR pigs, although no significant differences were found between the two groups. In the ileum, Megasphaera elsdenii and Mitsuokella multacida were significantly (P < 0.01) higher in LR pigs along with an increase of acetate and butyrate concentrations. Halomonas pacifica, Escherichia fergusonii, and Actinobacillus minor which belong to class Gammaproteobacteria were significantly lower (P < 0.01) in HR pigs with a significant increase (P < 0.01) of Lactobacillus acetotolerans-like bacteria. Therefore, the changed bacterial community may lead to a transformation of microbial function, such as the alteration of fermentation mode which is showed on the change of microbial metabolites like the concentration of short-chain fatty acids (SCFAs), to a response to the switch of dietary composition, and in turn, to help host absorb and utilize nutrients efficiently. The increase of dietary amylose induced the reduction of conditioned pathogens which may probably be due to the increase of some probiotics such as Lactobacillus, thus reducing the risk of intestinal disease.

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Nutrient and chemical sensing by intestinal pathogens

Cited by 17 publications

References 70 publications

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

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

Animal Models of EnterohemorrhagicEscherichia coliInfection

Responses in ileal and cecal bacteria to low and high amylose/amylopectin ratio diets in growing pigs

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