The impact of intestinal inflammation on the nutritional environment of the gut microbiota

Faber, Franziska; Bäumler, Andreas J.

doi:10.1016/j.imlet.2014.04.014

Cited by 80 publications

(67 citation statements)

References 60 publications

(69 reference statements)

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“…However, the Gammaproteobacteria taxa enriched in the proximal and distal small intestine during giardiasis are not the members of the Enterobacteriaceae that are often noted to bloom during gut inflammation (31,68). While the Enterobacteriaceae decreased in diversity, the diversity of the strictly aerobic Moraxellaceae and the Betaproteobacteria Rhodocyclaceae and Comomonadaceae increased.…”

Section: Figmentioning

confidence: 97%

“…In conjunction with direct effects on host tissues, Giardia could cause disruptions to the ecological health of commensal microbes in the gastrointestinal tract by altering the microbial composition, metabolic capacities, or chemical homeostasis in the gastrointestinal lumen. Other gut ecologically mediated diseases include infectious diseases with known bacterial pathogens (e.g., Clostridium difficile or Salmonella enterica serovar Typhimurium) and immune-mediated diseases wherein the entirety of the gut community appears perturbed in the absence of a dominant pathogenic species (e.g., Crohn's disease and irritable bowel disease [IBD]) (22,(31)(32)(33)(34). Similarly, the eukaryotic apicomplexan parasite Toxoplasma gondii has been proposed to act as a molecular adjuvant to the small intestinal microbiota, inducing acute ileitis (35).…”

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confidence: 99%

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Giardia Alters Commensal Microbial Diversity throughout the Murine Gut

et al. 2017

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Giardia lamblia is the most frequently identified protozoan cause of intestinal infection. Over 200 million people are estimated to have acute or chronic giardiasis, with infection rates approaching 90% in areas where Giardia is endemic. Despite its significance in global health, the mechanisms of pathogenesis associated with giardiasis remain unclear, as the parasite neither produces a known toxin nor induces a robust inflammatory response. Giardia colonization and proliferation in the small intestine of the host may, however, disrupt the ecological homeostasis of gastrointestinal commensal microbes and contribute to diarrheal disease associated with giardiasis. To evaluate the impact of Giardia infection on the host microbiota, we used culture-independent methods to quantify shifts in the diversity of commensal microbes throughout the gastrointestinal tract in mice infected with Giardia. We discovered that Giardia's colonization of the small intestine causes a systemic dysbiosis of aerobic and anaerobic commensal bacteria. Specifically, Giardia colonization is typified by both expansions in aerobic Proteobacteria and decreases in anaerobic Firmicutes and Melainabacteria in the murine foregut and hindgut. Based on these shifts, we created a quantitative index of murine Giardia-induced microbial dysbiosis. This index increased at all gut regions during the duration of infection, including both the proximal small intestine and the colon. Giardiasis could be an ecological disease, and the observed dysbiosis may be mediated directly via the parasite's unique anaerobic fermentative metabolism or indirectly via parasite induction of gut inflammation. This systemic alteration of murine gut commensal diversity may be the cause or the consequence of inflammatory and metabolic changes throughout the gut. Shifts in the commensal microbiota may explain observed variations in giardiasis between hosts with respect to host pathology, degree of parasite colonization, infection initiation, and eventual clearance.KEYWORDS Giardia, microbiome, parasite, pathogenesis G iardia lamblia is a microaerophilic protozoan parasite of humans and animals that causes significant morbidity and diarrheal disease worldwide (1, 2). Giardiasis is a zoonotic disease with diverse animal reservoirs. Parasites infect and complete their life cycle in mammalian hosts, and infected animals shed Giardia cysts into water supplies. Over 200 million people are estimated to have acute or chronic giardiasis, and rates of giardiasis approach 90% in areas where it is endemic (3, 4). When prevalent, giardiasis has been implicated as a primary cause of growth restriction for children, resulting in long-term consequences, such as stunting, failure to thrive, malnutrition, and cognitive disabilities (1, 2, 5). In addition, Giardia has been associated with substantial postclearance irritable bowel symptoms in both children and adults (1, 6-8). The significant and adverse impact of giardiasis on global human health contrasts with a considerable lack of resea...

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Section: Figmentioning

confidence: 97%

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confidence: 99%

Giardia Alters Commensal Microbial Diversity throughout the Murine Gut

et al. 2017

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“…Although this field of research is only at its infancy, it is exciting to consider role of pregnancy-associated changes in maternal gut microbiota composition influencing nutrient absorption, inflammation, microbial translocation as well as fetal gut colonization and metabolic tissue development in determining chronic disease risk. Gut microbial metabolism is modified by host inflammation; where the inflammatory host response creates a new metabolic niche, creating novel opportunities for potentially inferior microbes to thrive resulting in disruption of a balanced microbiota composition or dysbiosis (94). Whether an obesity-induced maternal pro-inflammatory environment is the result of, or the consequence of, fluctuating gut microbial populations is currently unclear.…”

Section: Resultsmentioning

confidence: 99%

Of the bugs that shape us: maternal obesity, the gut microbiome, and long-term disease risk

2014

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Chronic disease risk is inextricably linked to our early-life environment, where maternal, fetal, and childhood factors predict disease risk later in life. Currently, maternal obesity is a key predictor of childhood obesity and metabolic complications in adulthood. Although the mechanisms are unclear, new and emerging evidence points to our microbiome, where the bacterial composition of the gut modulates the weight gain and altered metabolism that drives obesity. Over the course of pregnancy, maternal bacterial load increases, and gut bacterial diversity changes and is influenced by pre-pregnancy-and pregnancy-related obesity. Alterations in the bacterial composition of the mother have been shown to affect the development and function of the gastrointestinal tract of her offspring. How these microbial shifts influence the maternal-fetal-infant relationship is a topic of hot debate. This paper will review the evidence linking nutrition, maternal obesity, the maternal gut microbiome, and fetal gut development, bringing together clinical observations in humans and experimental data from targeted animal models.

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“…Members of the Bacteroidetes and Firmicutes phyla are prevalent anaerobic bacteria in healthy individuals. Both metabolize nondigestible proteins and complex carbohydrates, such as gluten and fiber or mucus saccharides, respectively (75). In the absence of other sources, bacteria rely on fermentation of these carbohydrates and proteins to obtain the carbon and nitrogen that are essential to the biosynthesis of bacterial proteins, carbohydrates, lipids, and nucleotides.…”

Section: Bacterial Pathogenesis Controlled By Intestinal Chemical Senmentioning

confidence: 99%

“…Although reactive oxygen and nitrogen species are generated by the inflammatory host response during inflammation induced by S. Typhimurium, they oxidize luminal compounds (trimethylamine and thiosulfate), forming exogenous electron acceptors (trimethylamine N-oxide and tetrathionate) that can be used by S. Typhimurium (76). The presence of these acceptors enables facultative anaerobic bacteria, such as S. Typhimurium, to utilize microbiota-derived products to generate energy, balance redox reactions, and acquire carbon for the biosynthesis of other products essential to bacteria during infection (75).…”

Section: Bacterial Pathogenesis Controlled By Intestinal Chemical Senmentioning

confidence: 99%

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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The impact of intestinal inflammation on the nutritional environment of the gut microbiota

Cited by 80 publications

References 60 publications

Giardia Alters Commensal Microbial Diversity throughout the Murine Gut

Giardia Alters Commensal Microbial Diversity throughout the Murine Gut

Of the bugs that shape us: maternal obesity, the gut microbiome, and long-term disease risk

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

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